Thoracic II Flashcards
What are some general causes of hypoxia?
Common Causes
- Inadequate O2 supply (low FiO2)
- Hypoventilation
- V:Q inequities resulting from
- Atelectasis, compression, pulm edema
- Decreased O2 carrying capacity
- Related to anemia
- Left shift of O2-Hgb dissociation curve
- Caused by: hypothermia, decrease in 2,3 DPG (ie banked blood), alkalosis, hypocarbia.
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Review O2-Hgb curve
- Normal adult P50= 26.5 partial pressure of O2
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CADET faces RIGHT (right shift= release O2; left shift= love, hold onto O2)
- ⇑ CO2
- ⇑ Acidosis
- ⇑ DPG
- ⇑ Exercise
- ⇑ Temperature
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Review arterial O2 content calculation
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CaO2= (1.34 x Hgb x Sao2) + (PaO2 X0.003)
- remember Hgb most important portion of oxygen carrying capacity in blood
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CaO2= (1.34 x Hgb x Sao2) + (PaO2 X0.003)
What are some mechanisms of hypoxemia during anesthesia?
- Mechanical failure
- Most common cause:
- disconnect from 02 supply elbow of ETT (most common)
- followed by empty cylinders
- failure of pipeline (least common)
- Most common cause:
- Esophageal intubation
- Hypoventilation/hyperventilation
- Decreased FRC
- R to L Shunt
- Pulmonary embolism, ARDS
What are some potential hazards of O2 therapy?
- 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%
What are 3 main components for lung protective ventilation?
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low tidal volume (assumed to reduce stress and strain of the lung)
- (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
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recruitment maneuver (assumed to reopen any collapsed alveoli)
- breath hold at end inspiration to 20cmH2o for 15-20 seconds
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PEEP (assumed to keep a recruited lung open during ongoing anesthesia and surgery)
- 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.
What is peep and its effect? CPAP and its effect?
Positive-end expiratory pressure (PEEP)
- small positive A/W pressure at the end of expiration
- Uses
- Increases FRC
- Prevent A/W closure
- Improves oxygenation
- Aids ventilation in ARDS
Continuous positive airway pressure (CPAP)
- Positive pressure applied continuously to the A/W
- Uses
- S/P extubation to improve oxygenation
- Sleep disorders
- OLV to non-dependent lung
What are some physiologic considerations of one-lung ventilation?
- Hypoxic pulmonary vasoconstriction
- Lateral Decubitus Position
- Open Chest
- One-lung Ventilation
What is hypoxic pulmonary vasoconstriction?
- Local reaction occurring in hypoxic areas of the lung
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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
- thought to be able to decrease the blood flow to the nonventilated lung by 50%
- Onset and resolution are rapid based on changes in PaO2 (reflex initiated when PaO2<100mmHg)
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Occurs in 2 phases
- 1) initial phase within minutes
- 2)Delayed phase at 40 minutes
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Occurs in 2 phases
- 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)
What is the mechanism for hypoxic pulmonary vasoconstriction?
- 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
What are some factors that inhibit HPV?
- 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
- Nitrous Oxide has a clinically insignificant effect
- Usually okay at 1 MAC
- Vasoactive medications
- Vasodilators (inhibit HPV):
- Nitroglycerin,
- Nitroprusside,
- Dobutamine,
- Calcium channel blockers,
- B2 agonists (isoproterenol)
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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
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Volatile causes less inhibition of HPV when delivered to active site of vasoconstriction via pulmonary arterial blood than via alveolus
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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.
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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
What are some factors that decrease blood flow?
- Shunt is Increased by decreasing blood flow to the ventilated lung
- High mean airway pressures
- Low FiO2
- Vasoconstrictors
- Intrinsic PEEP
Review of preop evaluation for thoracic patient?
- 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
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Assess difficulty of lung isolation: examine chest radiograph and computed tomographic scan
- most useful predictor of difficult endobronchial intubaiton is chest imaging
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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
Considerations for premedication for thoracic cases?
- Typically avoided
- Small amount of short acting BZD if need for line placement
- Consider anti-sialogogue (Glycopyrolate)
- Can aid in visualization with FOB
- Empiric antibiotic coverage at induction (routine prophylaxis is Cephalosporin)
What might you need for the room setup for thoracic surgery?
- 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
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A-line: continuous BP and blood sampling
- ABGs on Room air and throughout case
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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%
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ETCO2 is less reliable indicator of PaCO2 during OLV than during TLV
- PaCO2 PETCO2 gradient tends to increase during OLV
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Need baseline PaO2 to help predict how they will do on OLV
- ABGs on Room air and throughout case
- CVP/ PA +/-
- 2 large bore IV’s are a MUST
- Sidestream spirometry- watch flow volume loops and I/E volumes
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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
What effect can OLV have on ETCO2 and PaCO2?
- ETCO2 is a less reliable indicator of PaCO2 during OLV than during TLV
- PaCO2- PETCO2 gradient tends to increased during OLV
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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
- 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
- it gives relative changes in perfusion of the two lungs independently during position changes and OLV
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PETCO2 is less directly correlated with alveolar MV during OLV, because PETCO2 also reflects lung perfusion and cardiac output
- 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
What monitoring may be indicated during thoracic cases?
- Pretty much everyone including healthy patients without special intra-operative conditions (ex. VATS)
- Arterial catheter
- We almost always do an art line- pretty much all thoracic surgery has a risk of great vessel/ heart compression
- Arterial catheter
- Add CVP +/- PA cath
- pneumonectomy cases, complex procedures, or redo thoracotomies
- may need for vasoactive gtt
- R IJ CVP preferred (lower risk pneumo)
- CVP unreliable in SVC syndrome
- also unreliable in lateral position with chest open
- pneumonectomy cases, complex procedures, or redo thoracotomies
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Sick patients with significant cardiopulmonary disease who will likely undergo further compromise with special intra-operative needs.
- patient with cor-pulmonale undergoing lobectomy or pneumonectomy
- Arterial catheter
- CVP + PA cath
- in lateral position with open chest, PA pressures are less accurate since we don’t know if tip lies in dependent of nondepednent lung
- Probably intra-op TEE
- mixed venous monitoring
Considerations for difficult airway in thoracic case?
- 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
Positioning keys for lateral decubitus position?
- 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
What are the ventilatory changes in lateral position?
V/Q Mismatch
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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
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Anesthetized but spontaneous breathing
- Nondependent lung better ventilated and dependent lung is better perfused (V/Q mismatch)
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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.
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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.
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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.
How do we prevent brachial plexus injury in the lateral position?
Factors that contribute to BP injury?
- 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
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The brachial plexus is the site of the majority of intraoperative nerve injuries related to the lateral position.
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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
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two varieties: the majority are _compression_ injuries of the brachial plexus of the _dependent_ arm
- Majority of nerve injuries resolve spontaneously over a period of months
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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
Head to toe assessment of patient in lateral position?
Anesthetic technique for thoracic surgery?
- GETA with PPV is safest method of anesthetizing patients
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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
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Intravenous Anesthetics
- Hemodynamic stability
- Does not diminish regional HPV
- diminish the need for high volatile dosages
Concerns for induction and maintenance thoracic anesthesia?
- 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.