Thoracic Flashcards

Question 1

Q

What are some complications from thoracic surgery?

What are patient risk factors for increased complications?

How can you decrease respiratory complications in high-risk patients?

Answer

A

Pulmonary morbidity: leading cause of complications following thoracic surgery
- Occurance: 15-20% thoracic sx pts
- Mortality: 3-4%
Cardiac: 10-15% thoracic sx patients
- Arrythmias: commonly atrial
- Ischemia → 5% (peak risk POD 2 & 3)
Other Complications:
- Atelectasis
- Pneumonia
- Respiratory failure (wean failure)
Patient Risk Factors:
- advanced age
- poor general health status
- COPD
- BMI > 30 kg/m2 (obesity)
- low FEV1
- low predicted postop FEV1
Decrease Respiratory Complications in HIGH RISK pts:
- Smoking cessation
- Physiotherapy prior to sx
- Thoracic epidural analgesia

Question 2

Q

What is a key question to ask prior to thoracic surgery?

What are 3 elements to preoperative assessment of lung function for thoracic cases?

Answer

A

Key question: Is this operable?
- Will the patient tolerate resection with acceptable risk?
3 elements:
- Lung mechanical function
  - Most valid test: Predictive Postop FEV1 (ppoFEV1)
    - Increased risk → < 30-40%
- Pulmonary parenchymal function
  - Most valid test: Predictive Postop Diffusing Capacity (ppoDLCO)
    - Increased risk → < 30-40%
      - Parenchymal tissue → “gas exchanging tissue”
- Cardiopulmonary reserve
  - Most valid test: Maximal Oxygen Consumption
    - Increased risk → < 15 ml/kg/min

Question 3

Q

Summary of the preop assessment?

What are the 4 m’s you should consider for cancer patients?

Answer

A

(4 things to consider prior to sx)

All patients: Assess
1. Exercise tolerance
2. Estimate ppoFEV1%
3. Discuss postop analgesia
4. d/c smoking
If ppoFEV1% < 40% pts:
1. Obtain testing →
  1. DLCO (diffusion capacity for carbon monoxide)
  2. V/Q scan
  3. VO2max
Cancer pts:
1. Consider the four M’s:
  1. Mass effects
  2. Metabolic effects
  3. Metastases
  4. Medications
    1. Ex:
      1. Bleomycin → use loest FiO2 and closely monitor oximetry
        exacerbates O2-inducted pulmonary toxicity
      2. Cisplatin → do not admin NSAIDs
        Elevation of serum creatinine
COPD pts:
1. Arterial blood gas
2. Physiotherapy
3. Bronchodilators
Increased renal risk:
1. Creatinine
2. BUN

Question 4

Q

How do we appropriately assess the respiratory system prior to thoracic surgery? What laboratory tests and diagnostics are pertinent?

Answer

A

History & Physical Examination
- Inspection, palpation, auscultation, percussion
Exercise tolerance:
- **primary determinant of outcome in older patients
  - Preop exercise capacity is BEST predictor of postthoracotomy outcome in older pts.
- Formal exercise testing required for:
  - Unable to give reliable history (or)
  - Limited ability to climb stairs bc comorbidities
    - ⇓ risk: Ability to climb > 3 flights
    - ⇑risk: unable to climb 2 flights
  - *QOL measures alone have poor correlation w/ FEV1, DLCO, and exercise testing and should not substitute actual testing → get testing
Laboratory Tests
- Routine labs
  - H/H
  - Coags
  - Chemistry
- sputum gram stain
- culture and cytology
- LFTs
- ABG’s
- Renal: BUN, Cr
  - Predictive factors for renal dysfx:
    - Preop HTN
    - ARBs
    - Hydoxyethel starch
    - Open thoracotomies
Diagnostics
- Chest Radiograph
- Pulmonary Function Testing
  - How operational or functional will the remaining lung be after resection.
- Pre-op bronchoscope → evaluate tumor/bx of bronchial nodes

Question 5

Q

What CXR findings have specific anesthesia implications?

Answer

A

CXR → MOST USEFUL predictor of DIFFICULT endobronchial intubation

Some radiographic findings have specific anesthesia implications:

Tracheal deviation and obstruction
- difficulty with intubation or ventilation
Mediastinal mass
- Ventilation difficulty → can compress AW
  - dangerous to cease spontaneous ventilation
- Superior vena cava syndrome
- PA compression
Pleural Effusions
- ⇓ VC
- ⇓FRC
Cardiac enlargement
- HF pts → don’t do well with one-lung vent d/t V/Q mismatching
  - susceptible to depressant effects of heart
Bullous cyst
- PPV → risk for pneumothorax
  - prone to rupture
Parenchymal reticulation consolidation (pneumonia)
- prone to atelectasis, edema, respiratory fx postop

Question 6

Q

What are some types of pulmonary function testing?

Answer

A

Classifications:
- Tests assessing abnormalities of gas exchange:
  - ARTERIAL BLOOD GAS- review interpretation
    - ROME
  - PULSE OXIMETRY- review
    - based on Beer Lambert law
      - Wavelength for pulse ox is 660 (deoxyhgb- red light) and 940 nm (oxyhgb- infrared light)
    - light emission frequencies
  - CAPNOGRAPHY- review phases of capnogram and normal and abnormal waveforms (see picture)
  - Ventilation Perfusion Scintigraphy: V/Q scan
    - Function/nonfunctional tissues
- Tests assessing mechanical dysfunction of lungs and chest wall (respiratory mechanics)
  - SPIROMETRY
    - Required for all patients undergoing pulmonary resection

Question 7

Q

What is the goal of spirometry?

Answer

A

Primary goal: recognize high or prohibitive risk pts for postop pulmonary complications
- ppoFEV1
- ppoDLCO
Identify patients who will benefit from aggressive perioperative pulmonary therapy
- Ex: maximal bronchodilators
- Smoking cessation
- Nutritional/exercise programming
Identify those in whom surgery should be avoided entirely
- Ex: ppoFEV1 or ppoDLCO = < 20%
  - High risk → think about R vs B (video assisted?)
NO single test or combination of tests will definitively predict which patients will develop postoperative pulmonary complications

Question 8

Q

What surgical patients need PFTs preop?

Why do we do PFTs?

Answer

A

WHO Needs PFTs ?

evidence of COPD
Smokers w/ persistent cough
Wheezing or Dyspnea hx
Restrictive Lung disease:
- Chest wall
- Spinal deformities
Morbidly obese
- esp. those with coexisting lung dx
Upper abdominal surgery candidates
Thoracic surgery candidates (open)
> 70 yo

Why Test?

Identifies patients with abnormal lung function

Improves the outcome of patients at risk
Reduces incidence of post-operative respiratory and ventilatory compromise
Resolves questions about resectability

Question 9

Q

What is forced vital capacity?

What is normal?

Answer

A

Maximal inspiration followed by rapid forceful exhalation
- Reflection → flow resistance in airway
  - Normal/Healthy pts → little/no difference b/t VC and FVC
    - Should be same in healthy patient!
  - Air trapping → major difference b/t VC and FVC
    - Small AW collapse and air trapping
Considerations:
- Exhalation → measured as a function of volume/time.
- Effort + cooperation dependent
Interpretation of % predicted:
- Normal: 80-120%
- Mild: 70-79%
- Moderate: 50%-69%
- Severe: < 50%

Question 10

Q

FRC in healthy lungs?

COPD?

Fibrotic lung?

Lung resection?

Answer

A

Healthy Lungs

Tidal volume (VT, usually 0.5 L) is inspired from the resting lung volume reached at end-expiration (FRC, 2.0 L).
With increased ventilation, as in exercise →
- VT is increased
- FRC may be reduced by approximately 0.5 L.

Old/COPD lungs → ⇑ FRC

FRC increases w/ age as elastic lung tissue is lost
→ this reduces lung recoil force countering the outward chest wall force → the lung assumes a higher volume.
The rate of this aging process is accelerated in COPD because of the contributions of chronic air trapping and marked loss of elastic tissue.

Fibrotic Lung Disease → ⇓ FRC

sometimes to 1.5 L

Lung Resection →⇓ FRC

Compensatory Emphysema → remaining lung will expand to fill the lung tissue void partially

Airway Obstruction

Exhalation is impeded such that inspiration commences before the usual resting lung volume is reached; thus end-expiratory volume is increased. Such air trapping reduces the resistance to gas flow in the narrowed airways, but because the lung tissue is hyperinflated and mechanically disadvantaged, the work of breathing overall is increased.

Question 11

Q

What is FEV1?

Answer

A

FEV₁ = forced expiratory volume in 1st second of FVC measurement
- Normal: 75-80% of FVC (declining with age)
  - Effort and cooperation dependent
Useful assessment!
- Good assessment for COPD severity
- Most valid test for postop respiratory complications: (equation)
  - ppoFEV1 %= preoperative FEV1 % × (1 −% functional lung tissue removed/100)

Question 12

Q

How is COPD categorized?

Answer

A

American Thoracic Society categorizes:

Stage I: FEV1 > 50% predicted
- Should not have significant dyspnea, hypoxemia, or hypercarbia
Stage II: FEV1 35-50%
Stage III: FEV1 < 35%.
- Stage II or III COPD → have an elevated PaCO2 at rest.

Question 13

Q

What is closing volume?

Answer

A

The lung volume at which airways begin to close or stop contributing to the expired gas
- Normal: 15-20% of VC
  - ** in healthy pt/sitting position**
- Smokers: ⇑ CV
  - Reflects loss of elastic recoil and/or small airway pathology

Question 14

Q

What is VO2max?

Answer

A

Maximum oxygen consumption (VO2max) during exercise testing
- ⇓ by 4% during exercise → high risk
Values:
- VO2max: > 20 ml/kg/min
  - Most have no pulm complications
- High risk → < 15 mL/kg/min (preop)
  - High M&M
- Very high risk → < 10 ml/kg/min
Testing: 6-minute test
- Requires little/no lab equipment
- VO2max can be estimated from 6-minute walk test: [distance walked (meters) / 30] = VO2max
  - 6 min walk (~450 m) → estimated VO2max = 450/30 = 15 mL/kg/min
    - Examples: VO2max
      - 5 flights = > 20 mL/kg/min
      - 2 flights = 12 mL/kg/min.
        ⇑ risk → SpO2 decrease > 4%

Question 15

Q

What is DLCO?

Answer

A

Diffusing Capacity (ppoDLCO)

Diffusing capacity (DLCO) is the ability of the lung to perform gas exchange (pt. inhales carbon monoxide and tested)
- High risk → < 40% of postop predicted value
  - correlates with both increased respiratory and cardiac complications
    - independent of FEV1 (even if FEV1 normal)
- DLCO (not FEV1) → negatively affected by preoperative chemotherapy
  - may be the most important predictor of complications in this subgroup of patients.
  - Some authors feel a higher cutoff risk-threshold for ppoDLco of < 50% may be more appropriate.
- Measured- CO inhalation

Question 16

Q

How do you predict postop pulmonary function?

Answer

A

One method of estimating the percent of functional lung tissue is based on a calculation of the number of functioning subsegments of the lung removed
- Right lung: 3 lobes
- Left lung: 2 lobes
Number of subsegments of each lobe is used to calculate the predicted postoperative (ppo) pulmonary function (picture →)
- ppoFEV1 = preop FEV1 (or DLco) % × ( 1 – segment % /100)
- Ex: After a RLL lobectomy
  - Taking 12 segments out of 42 segments → 12/42= 29%
    - Taking out 29% of total lung tissue
  - Equation:
    - Given: Preop FEV1 [or DLco] 70% of normal
    - 70% × ( 1 − 29/100) = 50% ppoFEV1
Postresection respiratory complications:
- ppoFEV1:
  - low risk = > 40%
  - risk = < 40% (complications)
  - high risk = < 30%
  - unacceptably high risk = < 20%

Question 17

Q

How do we estimate operative risk?

Answer

A

ALWAYS asses Functional Capacity
- Functional capacity > 2 METS → need spirometry
  - *ppoFEV1
  - *ppoDLCO
    - > 60% (both) → pt should do well
    - 30-60% → 6 min walk test (get VO2max)
  - 6 min walk test
    - Walk > 400 m → proceed to sx
    - Walk < 400 m → get exercise testing and formally calculate O2 consumption
      - > 10 ml/kg/min → increased risk
      - < 10 ml/kg/min → hold sx and optimize (consider video thoracoscopy)
Traditionally arterial blood gas data such as PaO2 less than 60 mm Hg or PaCO2 greater than 45 mm Hg have been used as cut-off values for pulmonary resection. Cancer resections have now been successfully done or even combined with volume reduction in patients who do not meet these criteria, although they remain useful as warning indicators of increased risk.

Question 18

Q

What factors characterize average risk? Elevated risk?

Answer

A

Average risk
- FEV1>2 L or 80% predicted
- PPO FEV1 >80$ predicted
- PPO FEV1 + PPO DLCO both >40%
- VO2 max >15 ml/kg/min
- ability to climb 3 flights stairs
Elevated risk
- FEV1 <2L or <40% predicted
- PPO FEV1 <40% predicted
- PPO DLCO <40% predicted
- VO2 max <10 mL/kg/min (on 6 min walk test)
- inability to climb one flight stairs
- o2 desat >4% during exercise

The National Emphysema Treatment Trial:

preoperative FEV1 or DLCO < 20% → unacceptably high perioperative mortality rate.
- These can be considered as the absolute minimal values compatible with a successful outcome.

Question 19

Q

Preop eval of patients for pulmonary sx?

Answer

A

Evaluate comorbidities
- Smoking related complications (CAD?)
- Cor pulmonale
- Paraneoplasm effects
  - Secreting hormones?
- CV dx
  - MI w/in 6 wks?
- Chemo
EKG/CXR
Labs
Lung function testing:
- FEV1 and DLCO
- VO2max
COPD → blood gas and response to bronchodilators

Question 20

Q

CV preop eval for pulmonary patients?

Answer

A

Cardiac complications are the second most common cause of peri-operative morbidity and mortality
- Elective pulmonary resection is considered “intermediate risk” for cardiac morbidity
CAD secondary to smoking may lead to ischemia
- Risk of post-thoracotomy ischemia = 5% (peaks POD 2 & 3)
Arrhythmia risk:
- 30-50% → post op arrhythmia after pulmonary resection (1^st week highest risk)
  - Most common: A-fib (60-70%)
- β-Adrenergic blockers → most effective drug to prevent arrhythmias
  - Caution: Concerns regarding use in reactive airways diseases.
- Diltiazem (CCB) → most useful drug for postthoracotomy arrythmia prophylaxis

Question 21

Q

What factors increase arryhtmia risk around pulmonary surgery?

Answer

A

Factors effecting increased arrythmia incidence:
- Extent of lung resection
  - pneumonectomy- 60%
  - lobectomy- 40%
  - nonresection thoracotomy- 30%
- Intrapericardial dissection
- Blood loss intraop
- Age (older)
- Extrapleural pneumonectomy
Two factors in the early postthoracotomy period interact to produce atrial arrythmias:
- (1) increased flow resistance through pulmonary vascular bed bc of permanent (lung resection) or transient (atelectasis, hypoxemia) causes with attendant strain on the right side of the heart
- (2) increased sympathetic stimuli and oxygen requirements
  - maximal on 2^nd postop day as patients become more mobile
Considerations:
- COPD pts → more resistant to pharmacologic-induced HR control when they develop posthoracotomy a fib
  - Require multiple drugs
Most common arrhythmia → Atrial fib/flutter
- Due to atrial stretch
Contributing factors
- Greater incidence in patients > 60 years old
- Surgical procedure: Left pneumonectomy (Right makes more sense?)
Prophylaxis:
- Digoxin
- Diltiazem/Verapamil/CCB’s
- Beta blockers- Esmolol
- Amiodarone

Question 22

Q

What are some recommendations for prevention of postop a fib in thoracic sx?

Answer

A

Consider those at highest risk for A fib:
- anterior mediastinal mass
- Lobectomy
- Pneumonectomy
- Esophagectomy
  - Diltiazem (if preserved CV fx and not taking BB)
  - Amiodarone
  - Statins
All patients:
- Continue BB preop
- Magnesium level
  - Optimize

Question 23

Q

What is the CV response to COPD and CAD?

Consideration for tmanagement in thoracic surgery patients?

Answer

A

CV response to COPD & CAD → pHTN
Pulmonary hypertension- 40-50% pts w/ severe lung disease
- Increased pulmonary vascular resistance
- Right ventricular hypertrophy and dilation
- LV dysfunction due to CAD, MI, HTN
Vascular Resistance measurements – PA, PAOP/PCWP, C.O., PV Compliance
- PAP (pulm artery pressure) > 25 or systolic >35:
  - Increased risk respiratory complications
  - prolonged intubation
Management:
- ECG/ECHO
  - Needed to determine severity of associated CV disease/pulm HTN
- AVOID HoTN
  - *vasopressin to maintain BP
After pulmonary resection → right ventricular dysfunction proportional to the amount of functioning pulmonary vascular bed that has been removed.
- The exact etiology and duration of dysfx unknown.
- Hemodynamic problem minimal when the patient is at rest
  - Dramatic when exercises → leading to:
    - elevation of pulmonary vascular pressures
    - limited CO
    - absence of normal decrease in PVR usually seen with exertion

Management of pHTN secondary to Lung Disease (chart →)

2 main types of pHTN we focus on:
- pHTN d/t left heart disease
- *pHTN d/t lung disease
  - noncardiac surgery more likely to have pHTN due to lung disease
Paravertebral blocks preferred over thoracic epidural in this population
1. May need PA cath to monitor pressures (CO)

Question 24

Q

What can be done preoperatively to help prevent respiratory complications in thoracic sx patients?

Answer

A

Stop Smoking
Dilate Airways
- B2-sympathomemitic
- Phosphodiesterase inhibitors
- Inhaled anticholinergics and/or steroids
Mucolytics
- Loosen/Remove Secretion
Treat infections
Nutrition/exercise/physiotherapy: Measures to increase motivation and postoperative care
- Chest physiotherapy → improve exercise tolerance if > 1 mo
  - little improvement if < 1 mo

Question 25

Q

What are come cardiac and respiratory effects of smoking?

Smoking cessation guidance prior to surgery?

Answer

A

Cardiac effects of smoking:
- Risk factor for developing CV dx
- Carbon monoxide →
  - decreases O2 delivery
  - increases myocardial work
- Releases catecholamines → coronary vasoconstriction
- Exercise capacity decreases
Respiratory effects of smoking:
- Risk factor for developing pulm dx
- Mucocilliary activity decrease
- Hyperreactive AW
- Pulm immune fx decrease
Smoking cessation:
- > 4 wks d/c smoking → Pulmonary complications⇓
- > 12 hrs d/c smoking → Carboxyhgb [] ⇓
  - There is no rebound increase in pulmonary complications if patients stop for shorter (< 8 weeks) periods before surgery. Intensive smoking-cessation interventions are the most successful.
- Important to avoid smoking postop
  - Smoking leads to prolonged period of tissue hypoxemia.
  - Wound tissue oxygen tension correlates with wound healing and resistance to infection.

Question 26

Q

What are some common COPD meds patients may be taking?

Answer

A

B adrenergic agnoists (ie albuterol, terbutaline)
- increase adenylate cyclase-→ increase cAMP→ decrease smooth muscle tone→ bronchodilation
Methylxanthines (ie aminophyllin, theophylline)
- phosphodiesterase inhibition→ increase cAMP→ potentiates endogenous catecholamine
  - improve diaphragmatic contracility, central respiratory stimulant
Corticosteroids (ie methylprednisolone, dexamethasone, cortisol)
- antiinflammatory, membrane stabilizing, inhibits histamine release
- potentiates b agonists
Anticholinergic (ie glyco, ipratropium)
- blocks acetylcholine at postganglionic receptors, decrease cGMP, relaxes airway smooth muscle
Antileukotriene (ie montelukast)
- inhibit leukotriene production
  - antiinfallmatory
  - used in addition to steroids

Question 27

Q

What is the classification, assessment and pathological manifestations of obstructive disease?

Answer

A

Classification: Chronic Bronchitis and Emphysema
- Causative Factors:
  - Tobacco Abuse - MAJOR
  - Alpha₁ antitrypsin deficiency→emphysema in young patients
- Manifestation: impairment of expiratory flow
  - Retention of gases
- Patho (from coexist)
  - Preventable/treatable dx characterized by progressive airflow limitation
    - decrase in elastic recoil
    - decrease in bronchiole wall rigidity
    - active bronchospasm
    - increase gas flow velocity
    - increase in goblet cell hypertrophy
Assessment of severity based on FEV₁ % of predicted values
- stage I: > 50% predicted
- stage II: 35 - 50%
- stage III: < 35%.
  - Stage I patients should not have significant dyspnea, hypoxemia, or hypercarbia, and other causes should be considered if these are present.
  - Stage II and III → do have those symptoms
Pathological manifestations:
- CV:
  - RV dysfunction (up to 50% COPD pts)
- Pulm:
  - Increased dead space ventilation
    - result in diversion of inspired air into (nonobstructed) ventilated, but poorly perfused, regions of lung.
  - Increased FRC
  - gas trapping
  - flow limitation
  - Stage II or III → increased CO2 at rest

Question 28

Q

Anesthetic management for patients with COPD?

Answer

A

Management:
- Preop: ALL COPD patients should have maximal bronchodilator therapy
- Need to admin O2 postop d/t unavoidable fall in FRC
  - The attendant rise in Paco2 should be anticipated and monitored (blood gases)
- Dysfunctional right ventricle → poorly tolerant of sudden increase in afterload
  - Ex: change from SV to controlled ventilation → compromised RV fx
    - RV fx becomes critical in maintaining CO as pulmonary artery pressure rises.
    - RV ejection fraction does not increase with exercise in COPD patients as it does in normal patients. Chronic recurrent hypoxemia is the cause of the RV dysfunction and the subsequent progression to cor pulmonale.
- Bullae:
  - Normal SV → intrabulla pressure slightly negative in comparison to surrounding parenchyma
  - PPV → pressure in bulla becomes positive in relation to adjacent lung tissue
    - Bulla expands w/ attendant risk of rupture, tension pneumo, and bronchopleural fistula
      - OK to do PPV → but keep aw pressures low
        
        high suspicion of pneumo
        
        have equipment ready for chest drain/one lung isolation if necessary
- Auto-PEEP:
  - Auto-PEEP becomes even more important during mechanical ventilation.
    - Directly proportional to TV
    - inversely proportional to expiratory time.
      - Allow for adequate expiratory time
  - Auto-PEEP has been found to develop in most COPD patients during one-lung anesthesia
Patients with obstructive disease → risk for both intraoperative & post-operative pulmonary complications
- GOAL: Minimize the risk of postop respiratory failure.
  - VA blunt airway reflexes and reflex bronchoconstriction (bronchodilation)
    - → consider the CV effects
Judicious use of opioids – prevent and/or treat postop pain but avoid respiratory depression.

Question 29

Q

Should you administer extra oxygen to COPD patients? Why or why not?

Answer

A

Previously thought chronically hypoxemic/hypercapnic patients relied on hypoxic stimulus for ventilatory drive and became insensitive to Paco2.
- This explained the clinical observation that COPD patients in incipient respiratory failure could be put into a hypercapnic coma by the administration of a high concentration of oxygen (FiO2).
- In actuality, only minor fraction of increase Paco2 in such patients is caused by a diminished respiratory drive, bc minute ventilation is basically unchanged.
  - The Paco2 rises because a high FiO2 causes a relative decrease in alveolar ventilation and an increase in alveolar dead space and shunt by the redistribution of perfusion away from lung areas of relatively normal ˙ V/˙ Q matching to areas of very low ˙ V/˙ Q ratio because regional hypoxic pulmonary vasoconstriction (HPV) is decreased and also as a result of the Haldane effect.
  - However, supplemental oxygen must be administered to these patients postoperatively to prevent hypoxemia associated with the unavoidable fall in functional residual capacity (FRC). The attendant rise in Paco2 should be anticipated and monitored. To identify these patients preoperatively, all stage II and III COPD patients need an arterial blood gas analysis.

Question 30

Q

What is one precaution to be mindful of during induction on COPD patients?

Answer

A

At risk for hemodynamic collapse with positive pressure manual ventilation via bag valve mask.

Severely flow-limited patients are at risk for hemodynamic collapse with the application of positive-pressure ventilation because of dynamic hyperinflation of the lungs. Even the modest positive airway pressures associated with manual ventilation with a bag/mask at induction can lead to hypotension because these patients have no increased resistance to inspiration but a marked obstruction of expiration. In some of these patients, this has contributed to the “Lazarus” syndrome, in which patients have recovered from a cardiac arrest only after resuscitation and positive-pressure ventilation were discontinued

Question 31

Q

Empysema vs bronchitis?

Answer

A

Emphysema

PaO_2: >60
PaCO_2: Normal
Appearance:
- Thin, anxious, purse lips
Accessory muscles
Dyspnea
Scant secretions
Markedly diminished breath sounds
With resp infx r-sided heart compromise
CXR: hyperinflation low diaphragm

Bronchitis

PaO₂< 60
PaCO₂ > 45
Appearance:
- Overweight, cyanosis dusky appearance
- “Blue bloater”
Cough
Copious secretions
Diminished breath sounds
R-sided heart failure /cor pulmonale
CXR: bronchovascular markings

Question 32

Q

Ventilation recommendations for obstructive dx?

Answer

A

Controlled ventilation
- slower frequency 6-10 bpm
- Larger TV
- keep PIP <40 cm H2O
- longer Expiration time to minimize V:Q mismatch
  - Ventilator setting:
    - larger TV
    - slower RR
    - longer I:E ratio
Considerations:
- Judicious use of opioids
- No N2O
  - due to risk of bullae
- Regional techniques with sensory above T6 are not recommended

Question 33

Q

Regional versus general considerations for patient with obstructive dx

Answer

A

Regional
- –Good choice extremity surgery, +/- lower abdominal; consider that patient can not tolerate additional IV sedation
- levels >T6 should be avoided as they need their accessory muscles!
General –
- IV administration of opioids and lidocaine prior to airway instrumentation will decrease reactivity
  - Increased risk bronchospasm
- No specific agent ‘ideal”-consider co-morbidities
- VA produce brochodilation and are rapidly eliminated
- Short acting NMB
- Judicious opioid use → resp depression
- Less tolerance for respiratory depressant effects of all drugs
  - Ex: benzos, opioids
- Humidification and low gas flow → for thick/dry secretions

Question 34

Q

Maintenance and emergence for obstructive lung dx?

When might a patient need to stay intubated postop?

Answer

A

Maintenance
- Ventilation
  - Tidal volumes
    - keep airway pressure < 40 cm/h20
    - 6-8 ml/kg
  - Slow rate (6-10 breaths per minute)
  - Sufficient time for exhalation
  - Be aware of pulmonary barotrauma, rupture of bullae, and auto-PEEP
  - Consider baseline PaCO2 a rapid correction to “normal values” may result in metabolic alkalosis
  - Spontaneous ventilation → may result in hypercapnia
    - Bad for RHF
Emergence
- Post-operative respiratory status is the priority issue
  - Calm and awake
- Adequate pain control (pain free breathing and improved coughing)

Extubation

Postop mechanical ventilation → risk patients
- Preop FEV1/FVC ratio < 0.5
- Preop PaCO2 > 50
Post-op mechanical ventilation should be to maintain
- PaO2 60-100
- PaCO2 - maintain pH 7.35-7.45

Question 35

Q

Asthma patho?

Answer

A

Airway hyper-responsiveness and inflammation
- Patho: Eosinophils, mast cells, neutrophils, macrophages, basophils, T lymphocytes have all been implicated as histologic mediators
Other probable mediators of acute bronchoconstriction
- include: cytokines, interleukins (3,4,5), arachidonic acid metabolites (leukotrienes and prostaglandins), kinins, histamine, adenosine, and platelet activating factor

Question 36

Q

Common drugs to treat asthma and MOA?

Question 37

Q

Asthma nad anesthetic techniques?

Answer

A

Consider regional techniques
GA →
- depress airway reflexes
- avoid hyperactivity &bronchoconstriction
Techniques:
- B2 Agonists via inhaler q 15-20 min or continuous neb
- Intravenous corticosteroids
  - Cortisol 2 mg/kg followed by 0.5 mg/kg/hr (or)
  - Methylprednisolone 60-125 mg q6 hr
- Supplemental O2 to maintain Sao2 > 90%
- IV magnesium sulfate may improve lung function
- Oral leukotriene inhibitor
- Tracheal intubation and mechanical ventilation (when Paco2 > 50 mm Hg)
- Bronchodilation via:
  - VA
  - Ketamine
- High gas flows → permit short inspiration times and longer expiration times.
  - Expiration time → prolonged to avoid air-trapping and “auto PEEP.”
- Permissive hypercarbia to avoid barotrauma.
- Empirical broad-spectrum antibiotics
What interventions would you take to meet those requirements?
How do you manage intraoperative bronchospasm?

Question 38

Q

Small cell lung cancer?

Answer

A

Poor prognosis
- Metastatic on presentation
- Prognosis: ~3 months after diagnosis due to metastasis
  - Not usually surgical candidates
  - Chemo/ radiation
- Neuroendocrine origin (paroneoplastic syndrome)
  - Lambert-Eaton Myasthenic Syndrome
    - impaired release of acetylcholine from nerve terminals
      - → typically presents as proximal lower limb weakness and fatigability that may temporarily improve with exercise.
    - Diagnosis:
      - confirmed by electromyography showing increasing amplitude of unusual action potentials with high-frequency stimulation
    - Considerations:
      - Similar to true myasthenia gravis → pt’s with myasthenic syndrome are extremely sensitive to nondepolarizing muscle relaxants. However, they respond poorly to acetylcholinesterase inhibitors (neostigmine)
      - subclinical involvement of the diaphragm and muscles of respiration
        ** think long term smoker w/o recovery from NMB → prob tumor/LEMS
      - Thoracic epidurals used w/o complication
      - NM fx resolved after tumor resection
  - SIADH → hyponatremia (most common)
    - Inappropriate production of antidiuretic hormone
  - Cushings & Hypercortisolism
    - through ectopic production of adrenocorticotropic hormone

Carcinoid tumors (SCLC tumors are the most malignant form of carcinoid tumors):

severe hypotension that may not respond to the usual vasoconstrictors (Refractory HoTN)
- will require use of specific antagonists octreotide or somatostatin.

Question 39

Q

Non-small cell lung cancer?

Answer

A

Includes: 75-80% primary lung ca
- squamous cell
  - slow growing
  - late metastases
  - frequently have sx due to large endobronchial mass
    - → SVC syndrome; mainstem bronchus involvement
    - hypercalcemia (due to elaboration of paraythroid-like factor and not due to bone mets)
- Adenocarcinoma (most common)
  - peripheral tumors
  - frequently metastasize early to brain, bone, liver, adrenals; extrapulmonary invasion is frequent (chest wall, diaphragm, pericardium)
Prognosis is variable
Surgery is usually considered
5 year survival is ~40%
- Without surgery <10%

Question 40

Q

4m’s to consider with lung Ca??

Question 41

Q

PE S/S, treatment

Answer

A

Signs & Symptoms:
- Acute dyspnea, tachypnea, pleuritic chest pain, cough, accentuation of pulmonic 2^nd sound, rales, tachycardia, fever, hemoptysis
Diagnosis: V:Q scan and/or pulmonary arteriography
ABG → Decreased PaO₂ and PaCO₂
Under anesthesia will see:
- arterial hypoxemia
- hypotension
- tachycardia
- bronchospasm
Management: monitor cardiac filling pressures, avoid drugs that increase PVR, positive pressure ventilation
Treatment: Pulmonary artery embolectomy, IVC filter, anticoagulants, analgesics

Question 42

Q

Cor pulmonale s/s, treatment?

Answer

A

Right ventricular enlargement 2^° pulmonary hypertension
S & S:
- dyspnea, syncope, PA mean pressure >20, prominent “a” wave on CVP, can be overt right heart failure
Rx:
- decrease RV workload → digoxin, diuretics, supplemental O₂, vasodilators, antibiotics, anticoagulants
- don’t increase afterload
Anesthesia Considerations?
- avoid hypoxemia, hypotension, hypercarbia
- minimal positive pressure on BVM during induction

Question 43

Q

URI and anesthesia?

Answer

A

Viral most often
Usual recommendation: avoid elective procedures that require tracheal intubation
- → airway hyperactivity, bronchospasm and laryngospasm- are all greater risks during URI
Airway irritability may persist for weeks after
Routine case cancellation controversial especially in the Pediatric ENT population

Question 44

Q

What are some general causes of hypoxia?

Answer

A

Common Causes

Inadequate O₂ supply (low FiO2)
Hypoventilation
V:Q inequities resulting from
- Atelectasis, compression, pulm edema
- Decreased O₂carrying capacity
- Related to anemia
Left shift of O₂-Hgb dissociation curve
- Caused by: hypothermia, decrease in 2,3 DPG (ie banked blood), alkalosis, hypocarbia.
Review O2-Hgb curve
- Normal adult P50= 26.5 partial pressure of O2
- CADET faces RIGHT (right shift= release O2; left shift= love, hold onto O2)
  - ⇑ CO2
  - ⇑ Acidosis
  - ⇑ DPG
  - ⇑ Exercise
  - ⇑ Temperature
Review arterial O2 content calculation
- CaO2= (1.34 x Hgb x Sao2) + (PaO2 X0.003)
  - remember Hgb most important portion of oxygen carrying capacity in blood

Question 45

Q

What are some mechanisms of hypoxemia during anesthesia?

Answer

A

Mechanical failure
- Most common cause:
  - disconnect from 02 supply elbow of ETT (most common)
  - followed by empty cylinders
  - failure of pipeline (least common)
Esophageal intubation
Hypoventilation/hyperventilation
Decreased FRC
R to L Shunt
Pulmonary embolism, ARDS

Question 46

Q

What are some potential hazards of O2 therapy?

Answer

A

Hypoventilation
- Leads to CO2 retention → hypoventilation in pts with COPD
Oxygen toxicity-
- Avoid FiO2 100% for periods >12 hours
- 80% >24H
- 60%>36H
- Can cause:
  - sub-sternal pain,
  - mild carinal irritation,
  - cough,
  - impairment of ciliary motion,
  - alveolar epithelial damage
  - interstitial fibrosis
Retrolental fibroplasia
- Newborns with high concentration of O2
Fire hazard
- Oxygen supports combustion
Absorption Atelectasis
- Atelectic shunting due to sum of the partial pressures in alveolar gas (760mmHg) greatly exceeds the pressure venous blood (147mmHg), gases diffuse into the blood and a rapid collapse of the alveoli occurs
Free radical damage from hyperoxia which can be damaging at cellular level
FiO₂ = fraction of inspired gas mix that is O₂
Clinical Goal = SaO2 >90%

Question 47

Q

What are 3 main components for lung protective ventilation?

Answer

A

low tidal volume (assumed to reduce stress and strain of the lung)
1. (1) low tidal volume, a small tidal volume is reasonable, and a volume of 6 to 8 mL/kg/body weight, as is generally suggested, is the same size of what a normal subject is breathing spontaneously when awake
recruitment maneuver (assumed to reopen any collapsed alveoli)
1. breath hold at end inspiration to 20cmH2o for 15-20 seconds
PEEP (assumed to keep a recruited lung open during ongoing anesthesia and surgery)
1. PEEP, opening up and keeping the lung open is also reasonable and even important. Both a recruitment maneuver and PEEP will achieve this.

These three tools have been adopted from intensive care, and one may ask whether they are equally useful in the mechanically ventilated, essentially lung healthy, anesthetized patient.

Question 48

Q

What is peep and its effect? CPAP and its effect?

Answer

A

Positive-end expiratory pressure (PEEP)

small positive A/W pressure at the end of expiration
Uses
1. Increases FRC
2. Prevent A/W closure
3. Improves oxygenation
4. Aids ventilation in ARDS

Continuous positive airway pressure (CPAP)

Positive pressure applied continuously to the A/W
Uses
1. S/P extubation to improve oxygenation
2. Sleep disorders
3. OLV to non-dependent lung

Question 49

Q

What are some physiologic considerations of one-lung ventilation?

Answer

A

Hypoxic pulmonary vasoconstriction
Lateral Decubitus Position
Open Chest
- One-lung Ventilation

Question 50

Q

What is hypoxic pulmonary vasoconstriction?

Answer

A

Local reaction occurring in hypoxic areas of the lung
Vasoconstriction in response to hypoxia in pulmonary arteries
- thought to be able to decrease the blood flow to the nonventilated lung by 50%
  - this prevents hypoxemia
  - precapillary vasoconstriction is helpful
Onset and resolution are rapid based on changes in PaO2 (reflex initiated when PaO2<100mmHg)
- Occurs in 2 phases
  - 1) initial phase within minutes
  - 2)Delayed phase at 40 minutes
Triggered by alveolar hypoxia, not arterial hypoxia
May be inhibited by calcium channel blockers, volatile agents and vasodilators
HPV is effective in ⇣ shunt flow (we like HPV with OLV)

Question 51

Q

What is the mechanism for hypoxic pulmonary vasoconstriction?

Answer

A

Exact mechanism is unclear
Hypoxia induced vasoconstriction in pulmonary vessels is different from other vessels which vasodilate in the presence of hypoxia
Possible mechanism
- Due to direct action of alveolar hypoxia on pulmonary smooth muscles sensed by the mitochondrial electron chain with reactive O2 species serving as a second messenger to increase calcium and smooth muscle vasoconstriction
- Endothelial derived molecules modulate the primary response
- Other humoral and neurogenic influences are probably involved

Question 52

Q

What are some factors that inhibit HPV?

Answer

A

Factors known to decrease Hypoxic pulmonary vasoconstriction and thus worsen the right to left shunting

Avoid drugs or events that will inhibit HPV:

Hypervolemia/hypovolemia
Excessive tidal volume or PEEP
Hypocapnia
Hypothermia
Acidosis
Volatile agents > 1 MAC
- Usually okay at 1 MAC
  - Nitrous Oxide has a clinically insignificant effect
    - Associated with increased postthoracotomy radiographic atelectasis in dependent lung compared to air/o2 mixture.
    - Avoid N2O during thoracic anesthesia
  - IV anesthetics minimal inhibition of HPV
Vasoactive medications
Vasodilators (inhibit HPV):
1. Nitroglycerin,
2. Nitroprusside,
3. Dobutamine,
4. Calcium channel blockers,
5. B2 agonists (isoproterenol)

At doses less than or equal to 1 MAC, modern VA (iso, sevo, des) are weak, equipotent inhibitors of HPV
- Inhibition of HPV response by 1 MAC of volatile is approximately 20% of total HPV response, and could only account for 4% net increase in total arteriovenous shunt during OLV, which it too small to be detected clinically
Volatile causes less inhibition of HPV when delivered to active site of vasoconstriction via pulmonary arterial blood than via alveolus
- During OLV, VA only reaches the hypoxic lung pulmonary capillary via mixed venous blood. No clinical benefit in oxygenation during OLV has been shown for TIVA
  - Sevo group had significantly less postop pulmonary complications and lower 1 year mortality.

Question 53

Q

What are some factors that increase shunt in ventilated lung?

Answer

A

Shunt is Increased by decreasing blood flow to the ventilated lung
- High mean airway pressures
- Low FiO2
- Vasoconstrictors
- Intrinsic PEEP

Question 54

Q

Review of preop evaluation for thoracic patient?

Answer

A

All patients: assess functional capacity, spirometry, discuss postoperative analgesia, discontinue smoking
Patients with ppoFEV1 or DLCO < 60%: exercise test
Cancer patients: consider the 4 Ms: mass effects, metabolic effects, metastases, medications
COPD patients: arterial blood gas, physiotherapy, bronchodilators
Increased renal risk: measure creatinine and blood urea nitrogen levels
Review initial assessment and test results
Assess difficulty of lung isolation: examine chest radiograph and computed tomographic scan
- most useful predictor of difficult endobronchial intubaiton is chest imaging
- distal airway problems may only be detected by CT.
  - can detect “saber-sheath” trachea, which can cause obstruction of tracheal lumen for a left-sided DLT during ventilation of dependent lung for a left thoracotomy
  - extrinsive or intrinsic compression of intraluminal obstruction of mainstem bronchus can interfere with placement and may only be evident with CT.
Assess risk of hypoxemia during one-lung ventilation

Question 55

Q

What might you need for the room setup for thoracic surgery?

Answer

A

Note frequent lateral position
- Must anticipate need for invasive monitoring at the outset
- Monitoring Requirements – based on degree of disease and the type of procedure
ECG, BP, pulse oximetry, temperature probe
I-stat for PaO2 and PaCO2 monitoring
A-line: continuous BP and blood sampling
- ABGs on Room air and throughout case
  - Need baseline PaO2 to help predict how they will do on OLV
    - Pao2 >400 with Fio2 1.0 is unlikely to desat during OLV
    - PaO2 of 200 is prone to desat during OLV although both may have SPO2 values of 99-100%
  - ETCO2 is less reliable indicator of PaCO2 during OLV than during TLV
    - PaCO2 PETCO2 gradient tends to increase during OLV
CVP/ PA +/-
2 large bore IV’s are a MUST
Sidestream spirometry- watch flow volume loops and I/E volumes
FOB and difficult airway cart in room
- Cook exchange catheter
TEE
- TEE that apply to thoracic surgery include hemodynamic instability (Fig. 53.11), pericardial effusions, cardiac involvement by tumor, air emboli, pulmonary thromboendarterectomy, thoracic trauma, lung transplantation, and pleuropulmonary disease
- On rare occasions, can detect undiagnosed PFO with reversal of flow caused by high peep intraop (causes increase RAP)
Non-invasive CO monitors???- unreliable with open chest
IV pumps for precise fluid/ pressor management
Consider CV drug box

Question 56

Q

What effect can OLV have on ETCO2 and PaCO2?

Answer

A

ETCO2 is a less reliable indicator of PaCO2 during OLV than during TLV
PaCO2- PETCO2 gradient tends to increased during OLV
- PETCO2 is less directly correlated with alveolar MV during OLV, because PETCO2 also reflects lung perfusion and cardiac output
  - it gives relative changes in perfusion of the two lungs independently during position changes and OLV
    - when turned lateral, PETCO2 of independent lung will fall relative to dependent lung, reflecting increased perfusion to dependent lung and increased deadspace to independent lung
      - however, excretion of CO2 will be higher from independent lung because of increased fractional ventilation
WIth onset OLV, PETCO2 of the dependent lung will fall transiently as all of the MV is transferred to this lung.
- THEN PETCO2 will rise as fractional perfusion to dependent lung increases due to collapse of lung and pulmonary vasoconstriction to nonventilated lung.
- If no correction in MV, then net result will be increased baseline PaCO2 and PETCO2 with increased gradient.
  - severe >5 mmHG or prolonged decreases in ETCO2 can indicate a maldistribution of perfusion b/w ventilated and nonventilated lung and may be early warning sign of patient that will desat during OLV

Question 57

Q

Considerations for difficult airway in thoracic case?

Answer

A

Always review AW/ thoracic assessment, history, xrays, and CT scans!
Concurrent cancer of the pharynx in the epiglottic area (5-8% of lung ca)
Radiation to head and neck
Previous aw surgery
Awake bronchoscopic exam before surgery if in doubt!
Establish AW with SLT in a difficult AW first before worrying about OLV; awake intubation is always an option
- Cook catheter exchange
- alternatively, can use SLT with bronchial blocker

Question 58

Q

Positioning keys for lateral decubitus position?

Answer

A

Axillary roll under torso caudal to axilla to prevent compression of neurovascular bundle and forward rotation of humeral head
hyper-abduction is prevented to keep brachial plexus from stretching
pulse ox or frequent palpation of radial pulse to ensure integrity of circulation to dependent arm
maintain head alignment to prevent compression jugular veins or vertebral arteries
- this can decrease cerebral circulation
typically induce in supine position
- inducing in lateral position may be indicated with bronchiectasis or hemoptysis until lung isolation achieved
when placed in lateral, can expect hypotension
- everytime resposition check oxygenation, ventilation, hemodynamic, line, monitor, and potential nerve injuries
- to minimize repositoning of tube, turn patients head, neck and endobronchial tube “en bloc” with patient thoracolumbar spine
pay careful attention to airway devices for robotic surgery. access to airway very difficult in middle of surgery

Question 59

Q

What are the ventilatory changes in lateral position?

Answer

A

V/Q Mismatch

Awake and spontaneous breathing
- Dependent (lower) lung is both better perfused and better ventilated, but lung volumes (FRC, VC, TV decrease)
- abdominal content dipslace diaphragm in cephalad direction
- dependent hemi-dieaphragm starts from high position, contraction of diaphragm leads to increased TV to fill dependent lung
- V/Q unchanged when awake
Anesthetized but spontaneous breathing
- Nondependent lung better ventilated and dependent lung is better perfused (V/Q mismatch)
- Anesthetized patient in the lateral position while the chest is not open and spontaneously breathing:
  - Dependent lung: decreased FRC, cephalad displacement of diaphragm by abdominal contents causes decreased FRC in dependent lung and decrease in zone 3. As the dependent lung’s FRC decreases, the volume and compliance also decreases.
  - FRC in nondependent (upper) lung - ventilation if preferentially distributed to nondependent lung, but blood flow is preferentially flowing to the dependent lung leading to a V/Q mismatch.
Anesthetized, mechanically ventilated patient
- Nondependent lung is overventilated and dependent lung is overperfused (worse V/Q mismatch)
- Large decrease in FRC
- Compression from abdominal viscera is no longer countered by force of contracting diaphragm.
- Ventilation is greater in the nondependent lung due to a path of least resistance causing a V/Q mismatch
  - Add PEEP to help restore FRC & improve V/Q

Anesthetized open chest:

Once the chest is opened, there is a decrease in the resistance of gas flow to the nondependent lung by detaching the lung from the pleural connection to the chest wall.
Decrease in ventilation to dependent lung.
Downward shift of mediastinum from loss of intrapleural pressure in nondependent lung.
Decrease ventilation to the dependent lung from the downward compression of the mediastinum structures.
Decreased CO & circulatory compromise.
Positive pressure ventilation minimizes these effects.

Question 60

Q

How do we prevent brachial plexus injury in the lateral position?

Factors that contribute to BP injury?

Answer

A

Axillary roll b/t chest wall and the bed just caudal to the dependent axilla (never IN the axilla)
Purpose: ensures weight of the thorax is borne by chest wall and to avoid compression on axillary neurovascular structures.
ALWAYS check pulse in dep arm
Never abduct more than 90 degrees, never extend posterior beyond neutral position, or anteriorly more than 90 degrees
The brachial plexus is the site of the majority of intraoperative nerve injuries related to the lateral position.
- - two varieties: the majority are _compression_ injuries of the brachial plexus of the _dependent_ arm
    - also a significant risk of _stretch_ injuries to the brachial plexus of the _nondependent_ arm
Majority of nerve injuries resolve spontaneously over a period of months
Traction injury of suprascapular nerve can cause deep, poorly circumscribed pain of posterior and lateral aspects of the shoulder.
- ensuring vertebral alignment from side of table can help prevent the whiplash syndrome

Question 61

Q

Anesthetic technique for thoracic surgery?

Answer

A

GETA with PPV is safest method of anesthetizing patients
Inhaled Anesthetics (benefits)
- Good Bronchdilators
- Obtund A/W reflexes
- Can be delivered with high O2 Concentrations
- Cardiovascular stable
- Rapidly eliminated
- Preserve HPV at 1 MAC
Intravenous Anesthetics
- Hemodynamic stability
- Does not diminish regional HPV
- diminish the need for high volatile dosages

Question 62

Q

Concerns for induction and maintenance thoracic anesthesia?

Answer

A

Smooth Induction; Anticipate reactive airway!
- Denitrogenate!
- DLT: frequent bronchospasm trigger
- Propofol or ketamine
Inhaled Anesthetics; Judicious Opioids
- Sevo may be the most potent bronchodilator
Thoracic Epidural Anesthesia; Paravertebral blocks
Minimize Nitrous Oxide (blebs; bullae)
PPV with Muscle Relaxation
Active warming
Maintain adequate cardiac output
Consider Dexmedetomidine infusion- improves oxygenation index and decreases shunt fraction in OLV
The principles of anesthetic management are the same as they are for any asthmatic patient: avoid manipulation of the airway in a lightly anesthetized patient, use bronchodilating anesthetics, and avoid drugs that release histamine.

Question 63

Q

Considerations for the administration of fluids in thoracic anesthesia?

Answer

A

Fluid Administration
- Prefer colloids vs crystalloids
Due to hydrostatic effects, excessive fluids can cause increased shunting and pulmonary edema
Recommend:
- Fluid should be limited to < 3L/first 24hours
- No fluid for third-space loss
  - May only give <1L fluid for entire VATS case

Question 64

Q

Recommended anesthetic technique for induction and maintenance of thoracic case?

Answer

A

Induction

Pre-oxygenate with 100% FIO2
Narcotic vs. opioid sparing
Induction agent
Non-depolarizing muscle relaxant (no histamine release)
Volatile agent and Lidocaine prior to intubation
Intubate
Position

Maintenance

Inhaled anesthetic
Opioid vs. opioid sparing
Non-depolarizing muscle relaxant
Controlled ventilation
Extubation vs Tube change

Answer 63

A

Epidural analgesia – preferred technique
Paravertebral blockade– block five interspaces: two above and two below plus at the site
Parental Narcotics – use judiciously, PCA
Ketorolac/ NSAIDs as a supplement
- preferred to help with shoulder pain
Other multimodal strategies- see previous slide
Options: neuraxial blockade, paravertebral blocks, and antiinflammatories preferred to narcotic-based analgesia. However, only epidural techniques have been shown to consistently have the capability to decrease postthoracotomy respiratory complications in high-risk patients.2 Continuous paravertebral blockade may offer comparable analgesia with a lower rate of block failure and fewer side effects
Epidural and heparin/ LMWH:** ASRA guidelines suggest an interval o**f 2 to 4 hours before or 1 hour after catheter placement for prophylactic heparin administration.** Low-molecular-weight heparin (LMWH) recommendations and precautions are: (**1) a minimal interval of 12 hours after low-dose LMWH and (2) 24 hours after higher-dose LMWH before catheter placement.

Answer 64

A

Indication
- selective atelectasis of the lung being operated on
- Absolute*
  - Isolation to avoid spillage or contamination
  - Control of the distribution of ventilation
  - Unilateral bronchopulmonary lavage for pulmonary alveolar proteinosis
- Relative
  - High vs. lower priority surgical exposure
  - Severe hypoxemia due to unilateral lung disease
Separation via 3 methods
- Double Lumen Tubes
- Bronchial Blockers
  - More common in peds
- Endobronchial Tubes
  - Least common
Management
- Operative lung CPAP
- Non-operative PEEP
Key point here is that one lung is not ventilated but is still perfused leading to a shunt

Answer 65

A

Normal Blood Flow Distribution lateral decubitus position = 40:60 (NONDEP: dependent)
OLV Blood Flow with HPV = 20:80 – a 50% HPV response
1 MAC ISO inhibits HPV by 21%
Blood Flow 24:76 – INCREASE intrapulmonary shunt by 4%
Causes a Right-to-Left Intrapulmonary Shunt
- Decreased by HPV
Check ABG before OLV and 20 minutes after initiating OLV
- CO₂ elimination usually not affected if Ve (minute ventilation) is unchanged
- Likely to see a transient fall in ETC02 and then rise as we correct minute ventilation of OLV
Several inhaled—but not intravenous—anesthetics inhibit HPV in isolated lung preparations.
Studies with no obvious changes in cardiac output indicated that isoflurane and halothane depress the HPV response by 50% at a minimum alveolar concentration (MAC) of 2

Answer 66

A

Factors to correlate with increased risk for desaturation during OLV
- High percentage of ventilation or perfusion to operative lung as seen on preoperative scan
  - During one-lung ventilation (OLV) for thoracotomy or thoracoscopy there is an obligate 20% to 30% shunt through the nonventilated lung.
  - If the operative lung has little perfusion preoperatively because of unilateral disease, the patient is unlikely to desaturate during OLV.
  - Finally, the degree of obstructive lung disease correlates in an inverse fashion with PaO2 during OLV. Other factors being equal, patients with more severe airflow limitation on preoperative spirometry tend to have a better PaO2 during OLV than patients with normal spirometry.
- Poor Pa02 during 2-lung ventilation especially in the LDP*
  - >400 less likely to desat with OLV
  - <200, more likely to have trouble
- Right-sided thoracotomy
  - Larger lung mass
  - In a series of patients, the mean PaO2 during left thoracotomy was approximately 70 mm Hg higher than during right thoracotomy
- Normal preop spirometry or restrictive dx
- Supine positon during one-lung ventilation
Necessitates prophylactic measures
- CPAP to non-ventilated lung (2-5cmH20)
- PEEP to the ventilated lung
- Or both

Answer 67

A

Patient height is the best predictor of DLT size
- Small (4’6”- 5’3”) – 35-37 FR
Medium (5’3” – 5’7”) – 37 or 39 FR – most commonly used size
Tall (> 5’7”) – 41 FR
Proper size allows or 1-2 mm smaller than patients L bronchus to allow for space of bronchial cuff
DLT: Males are usually 39F and Females 37F.
Advantages of LEFT DLT: The right-sided DLT incorporates a modified cuff and slot on the endobronchial lumen that allows ventilation for the right upper lobe
In adults, depth, measured at the teeth, for a properly positioned DLT, will be approximately 12 + (patient height/10) cm

Answer 68

A

Usually a Left sided DLT is used.
Some reasons a Right DLT might be need (See table)
The anatomic differences between the right and the left mainstem bronchus are reflected in the fundamentally different designs of the right-sided and left-sided DLTs.
- the right mainstem bronchus is shorter than the left bronchus, and the right upper lobe bronchus originates at a distance of 1.5 to 2 cm from the carina,
  - techniques using right endobronchial intubation must take into account the location and potential for obstruction of the orifice of the right upper lobe bronchus.
  - The right-sided DLT incorporates a modified cuff and slot on the endobronchial lumen that allows ventilation for the right upper lobe.

Answer 69

A

Auscultation and bronchoscopy should both be used each time a DLT is placed and again when the patient is repositioned.
Breath-by-breath monitoring of inspired and expired tidal volumes gives early warning of accidental changes in the intraoperative position of a DLT or air leaks during pulm rsx
1^ST View through tracheal lumen
- Ensure no bronchial cuff herniation over the carina- should be 5- 10mm below carina
- Identify the take-off of the RUL bronchus through the tracheal view (3 orifices)
2^nd View through bronchial lumen
- Check patency
- Check orifices of both the left upper and lower lobes
Must have large hemostat or Kelly clamp in the room
If lung deflation not achieved despite proper positioning, can place suction to expedite lung deflation
The breath-by-breath monitoring of inspired and expired tidal volumes gives early warning of accidental changes in the intraoperative position of a DLT, with loss of lung isolation if the expired volume suddenly decreases (there is normally a 20- to 30-mL/ breath difference caused in part by the uptake of inspired oxygen).
The development of a persistent end-expiratory flow during OLV, which correlates with the development of auto-PEEP, can be seen on the flow-volume loop.91 Also, the ability to accurately measure differences in inspiratory and expiratory tidal volumes is extremely useful in assessing and managing air leaks during and after pulmonary resections.

Answer 70

A

A “3-step” method to confirm position of a left DLT by auscultation.

Step 1, During bilateral ventilation, the tracheal cuff is inflated to the minimal volume that seals the air leak at the glottis. Auscultate to confirm bilateral ventilation.
Step 2, The tracheal lumen of the DLT is clamped proximally (“clamp the short side short”) and the port distal to the clamp is opened.
- During ventilation via the bronchial lumen, the bronchial cuff is inflated to the minimal volume that seals the air leak from the open tracheal lumen port. Auscultate to confirm correct unilateral ventilation.
  - only need 0.6-0.7 mL in bronchial cuff! Only use 3 cc syringe

Step 3, The tracheal lumen clamp is released and the port is closed. Auscultate to confirm resumption of bilateral breath sounds.

Answer 71

A

Maintain two lung as long as possible
- During the period of two-lung anesthesia before the start of OLV, atelectasis will develop in the dependent lung.
  - It is useful to perform a recruitment maneuver to the dependent lung (similar to a Valsalva maneuver, holding the lung at an end-inspiratory pressure of 20 cm H2O for 15–20 seconds) immediately after the start of OLV to decrease this atelectasis. Recruitment is important to maintain PaO2 levels during subsequent OLV
TV (5-6 mL/kg of predicted body weight*)
PEEP 5-10 cm H2O (caution in patients with severe obstructive disease)
Respiratory rate (~12/min)to maintain PaCO2 between 35-40 mmHg
Maintain PIP to <35 cm H20
Plateau pressures <25 cmH20
Remember it is harder to maintain Pa02 than PaCo2
MUST have continuous monitoring of oxygenation and ventilation
Denitrogenate- very important: The gas mixture in the nonventilated lung immediately before OLV has a significant effect on the speed of collapse of this lung.
- Because of its low blood-gas solubility, nitrogen (or an air-oxygen mixture) will delay collapse of this lung
Titrate FiO2
A saturation>90% (PaO2 > 60 mm Hg) is commonly accepted (high 80’s for short intervals)
Consider Pressure Control Ventilation (PCV) esp for patients at risk for lung injury
- must watch the TVs closely as they can change suddenly
With the use of intravenous anesthetic techniques or volatile anesthetics at less than or equal to 1–minimum alveolar concentration (MAC) doses, hypoxemia during one-lung ventilation (OLV) occurs infrequently. The use of continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP) as treatment for hypoxemia during OLV should be guided by the individual patient’s lung mechanics.
The use of large tidal volumes during OLV (e.g., 10 mL/kg) can contribute to acute lung injury, particularly in patients at increased respiratory risk, such as after pneumonectomy.

Answer 72

A

Most common: malpositioning
- A malpositioned DLT will fail to allow collapse of the lung, causing gas trapping during positive-pressure ventilation, or it may partially collapse the ventilated or dependent lung, producing hypoxemia.
- A common cause of malposition is
  - dislodgment of the endobronchial cuff because of overinflation,
  - surgical manipulation of the bronchus, or
  - extension of the head and neck during or after patient positioning.
AW trauma or rupture
- Airway trauma can occur from an oversized DLT or when an undersized DLT migrates distally into the lobar bronchus and the main (i.e., tracheal) body of the DLT comes into the bronchus, producing lacerations or rupture of the airway.
- Airway damage during the use of DLTs can present
  - as an unexpected air leak,
  - subcutaneous** emphysema**,
  - massive airway bleeding** into the lumen of the DLT, **or
  - protrusion of the endotracheal or endobronchial cuffs into the surgical field, with visualization of this by the surgeon.
- If any of the aforementioned problems occur, a bronchoscopic examination and surgical repair should be performed.
Tension pneumothorax to ventilated lung during OLV

*

Answer 73

A

Causes of Hypoxemia:

Tube malposition
Bronchospasm
Decrease CO
Hypoventilation
Decrease FiO2
Pneumothorax of dependent lung

Treatment of hypoxia in olv

Check tube placement especially every position change with fiberoptic scope
Increase FIO2 to 100%
CPAP to nondependent, nonventilated lung (see notes)
Perform a recruitment maneuver of the ventilated lung. To eliminate any atelectasis inflate the lung to 20 cm H2O or more for 15 to 20 seconds- watch for hypotension
PEEP (5-10 cmH2O) to dependent, ventilated lung after recruitment
- Recruits collapsed airways, Increase compliance, increase FRC
Inform surgeon and go back to two lung ventilation
Ligation of pulmonary artery in pneumonectomy patients
Apneic oxygen insufflation to the nondependent lung.
- Application of 3 liters of O2, via a suction catheter to the nonventilated lumen of the DLT
ECMO as a last resort
Significant desaturation (SpO2 < 90%) during OLV occurs in 1% to 10% of the surgical population in spite of a high FiO2
CPAP with oxygen to the nonventilated lung is a reliable method to improve PaO2 during OLV.
- CPAP should be applied to an inflated (recruited) lung to be completely effective.
- The opening pressure of atelectatic lung regions is greater than 20 cm H2O and these units will not be recruited by simple application of CPAP levels of 5 to 10 cm H2O.
- When CPAP is applied to an inflated lung, levels of CPAP as low as 1 to 2 cm H2O can be used.
- Since the normal transpulmonary pressure of the lung at FRC is approximately 5 cm H2O, levels of 5 to 10 cm H2O CPAP applied to a fully recruited lung result in a large-volume lung that impedessurgery particularly during minimally invasive procedures.
- Lower FiO2 levels of CPAP are of clinical benefit and can be titrated to the ventilated lung in patients at risk of oxygen toxicity using an air/oxygen blender.

Answer 74

A

At completion, the surgeon will ask you to re-inflate the lung (while camera still in ideally)
- May also test bronchial stump (20 cmH20 pressure in circuit so they can see leaks)
Manually ventilate the patient up to 30 cm H20 until you see the lung re-inflated
Place the patient back on your original ventilation settings because you are now ventilating both lungs.
Chest Tube(s) will be inserted and the surgeon may want to know how much volume you are losing. If your tidal volume is set on 700 mLs and you are only getting back 400 mLs, you are obviously losing 300 mls.
- This should improve when the chest tube(s) is connected to suction.

Answer 75

A

Emergence and Extubation

Inflate lung to ~30 cm H₂O pressure
- to reinflate the atelectatic area and check for air leaks
Check Chest Tube patency
- Chest tube to water seal only
Prompt extubation
- if patient meets the necessary requirements and does not pose a risk for PPC
Switch to a single lumen ETT
- if needed for transfer to ICU
After lung resection surgery, it is usually possible to wean and extubate patients with adequate predicted postoperative respiratory function in the operating room provided they are “AWaC” (alert, warm, and comfortable).

Tracheal Extubation

Criteria:

Hemodynamic Stability
RR not greater than 20-30/min (adult) with normal PaCO2
Adequate PaO2 (>60) with FiO2 < 40-50% and PEEP < 5-10
Adequate mentation (GCS >13)
*Acute phase of disease is resolved and adequate cough is present

Answer 76

A

Mediastinoscopy
- is the standard method for the evaluation of mediastinal lymph nodes in the staging of NSCLC, to in the diagnosis of anterior/superior mediastinal masses, stage SCLC
2 to 3 cm is made in the midline of the lower neck in the suprasternal notch.
mediastinoscope inserted toward the carina
innominate artery immediately anterior to the mediastinoscope
- worried about compression
Anesthetic management of a patient with an anterior or superior mediastinal mass should be guided by the patient’s symptoms, the preoperative computed tomography (CT) scan, and the echocardiography findings.
Compression to innominate artery can cause poor flow to right carotid artery
- innominate artery supplies not only the right arm but also the right common carotid
- Poor Cerebral perfusion results
Central airway obstruction due to compression of the trachea may occur during induction of anesthesia or during the manipulation of the mediastinoscope near the trachea
Technique: GA with ETT and Controlled Ventilation
- Plan to extubate in the OR
Monitor a-line/ pulse OX on right arm
- if absent waveform ask surgeon to reposition mediastinoscope
BP on left
Morbidity related to mediastinoscopy ranges from 2% to 8%. The most severe complication of mediastinoscopy is major hemorrhage, which may require emergent thoracotomy. Other potential complications include airway obstruction, compression of the innominate artery, pneumothorax, paresis of the recurrent laryngeal, phrenic nerve injury, esophageal injury, chylothorax, and air embolism

Answer 77

A

Technique:
- General Anesthesia with OLV placed in left main stem bronchus
- Smooth IV induction and inhaled/ balanced anesthetic
- A-line
- Lateral decubitus position
Advantages :
- less post-op pain
- shorter hospital stay
- improved post-op pulmonary function
Post-op paravertebral blocks
Always possibility for conversion to open thoracotomy with massive bleeding

Answer 78

A

Tumors of the mediastinum include thymoma, teratoma, lymphoma, cystic hygroma, bronchogenic cyst, and thyroid tumors
Can cause obstruction of major airway or great vessels
- Obstruction often distal to ETT
- May be unable to forcibly pass ETT past obstruction
A history of supine dyspnea or cough = possibility of airway obstruction upon induction of anesthesia
MAINTAIN SPONTANEOUS VENTILATION until airway SECURED! (Awake intubation, inhalational induction or ketamine are options)
Rigid bronch must be available and surgeon must be at bedside for induction
ECMO is a rescue option with loss of AW

Answer 79

A

Cardiac herniation
Pulmonary torsion
Hemorrhage
Bronchial disruption
Resp insufficiency
Intra-op pulm edema
R heart failure
Neural injuries
- Phrenic nerve
- Vagus nerve
- Recurrent laryngeal nerve
- Spinal cord ischemia
Pain is also an issue pot-op
Shoulder Pain
Ipsilateral shoulder pain is very common after thoracic surgery. It has been documented in 78% of patients immediately postoperatively.357 In 42% of patients this pain was judged to be clinically relevant.
- By postoperative day 4, 32% of patients had shoulder pain, but only 7% had clinically relevant shoulder pain.
- Shoulder pain occurred after both open and VATS surgery; the incidence may be decreased after VATS.
- This pain was felt to be of two major types:
  - 1. Referred pain (55%). This is thought to originate from phrenic nerve afferent fibers and related to diaphragmatic or mediastinal irritation.
  - 2. Musculoskeletal (45%). This pain was associated with tenderness of the involved shoulder muscles and pain with movement.
    - Of the two types, the musculoskeletal pain was more intense and more difficult to treat.
- Shoulder pain is not treated by any of the common regional blocks performed for thoracic surgery (e.g., thoracic epidural analgesia, paravertebral block). Shoulder pain is most responsive to antiinflammatories. Phrenic nerve infiltration and interscalene brachial plexus block358 have had some success but carry a risk of causing diaphragm dysfunction.
Postthoracotomy Neuralgia and Chronic Incisional Pain In one prospective study, chronic postoperative pain at 6 months was documented in 33% of patients after thoracotomy and 25% after VATS.359
- In this study, chronic pain was not associated with preoperative psychosocial measurements found to correlate with chronic postoperative pain in other types of surgery.
- Chronic pain was associated with acute postoperative pain. This suggests that chronic pain after thoracic surgery may be partially preventable by intensive management of acute postoperative pain.

Answer 80

A

Zone 1
- dead space V>Q
- PA (alveolar) > pa (arterial)> pv (venous)
- Increased by HoTN, PE, high a/w pressure
- Improved by- bronchioles will contrict to minimize the ventilation to poorly perfused alveoli
Zone 2
- V=Q
- Pa >pA> pv
- blood flow proportional Pa to PA
- “waterfall”
Zone 3
- V > Q
- Shunt like, better perfused than ventilated
- Improved by HPV to reduce blood flow to poorly ventialted alveoli

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