16.2 Thoracic Anaesthesia, One-Lung Ventilation, and Major Vascular Surgery

16.2 Thoracic Anaesthesia, One-Lung Ventilation, and Major Vascular Surgery

Thoracic and major vascular procedures present extreme physiological stresses: the deliberate collapse of one lung creates profound ventilation-perfusion mismatch, while aortic cross-clamping imposes abrupt, massive alterations in cardiac afterload, organ perfusion, and metabolic homeostasis.

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1. Preoperative Assessment for Lung Resection Surgery

Surgical resection of pulmonary tissue (wedge resection, segmentectomy, lobectomy, pneumonectomy) irreversibly reduces the functional capillary surface area and ventilatory reserve. Preoperative assessment determines whether the remaining lung parenchyma will sustain gas exchange and prevent post-resection respiratory failure.

The Functional Segment Algorithm

The human lung contains 19 functional anatomical segments:

• Right Lung (10 segments): Upper lobe (3: apical, posterior, anterior), middle lobe (2: lateral, medial), lower lobe (5: superior, medial basal, anterior basal, lateral basal, posterior basal).
• Left Lung (9 segments): Upper lobe (3: apical, posterior and anterior; the apical and posterior segments are often fused as one apicoposterior segment), lingula (2: superior, inferior), lower lobe (4: superior, anteromedial basal, lateral basal, posterior basal).

The Predicted Postoperative (PPO) pulmonary function is calculated as: $\text{PPO-}FEV_1\% = \text{Preoperative }FEV_1\% \times \left(1 - \frac{S_{\text{resected}}}{19}\right)$ $\text{PPO-}DLCO\% = \text{Preoperative }DLCO\% \times \left(1 - \frac{S_{\text{resected}}}{19}\right)$ where $S_{\text{resected}}$ represents the number of functional, non-obstructed segments to be surgically removed. If a whole lung is non-functional (e.g. total atelectasis from an endobronchial tumour), its removal will not alter postoperative mechanics, as reflected by quantitative ventilation-perfusion scintigraphy ($V/Q$ scan).

          [ PHYSIOLOGICAL ASSESSMENT BEFORE LUNG RESECTION (ACCP 2013) ]
                                     |
              Calculate PPO-FEV1% and PPO-DLCO% (segment counting)
                                     |
       +-----------------------------+-----------------------------+
       |                             |                             |
  Both > 60%                 Either 30-60% (both > 30%)       Either < 30%
       |                             |                             |
  [ LOW RISK ]              Low-technology exercise test      Formal CPET
  No further testing        - Stair climb > 22 m, or               |
                            - Shuttle walk > 400 m                 |
                              -> LOW RISK                          |
                            If below these values -> CPET ---------+
                                                                   |
                    VO2peak > 20 mL/kg/min or > 75% predicted  -> LOW RISK
                    VO2peak 10-20 mL/kg/min or 35-75%          -> MODERATE RISK
                    VO2peak < 10 mL/kg/min or < 35%            -> HIGH RISK

Risk Stratification Guidelines (ACCP 2013 and ERS/ESTS 2009)

• ACCP 2013 (Brunelli et al., Chest):
  • Low Risk: Both $\text{PPO-}FEV_1\%$ and $\text{PPO-}DLCO\%$ $> 60\%$; expected operative mortality below about $1\%$, and no further testing is needed.
  • Either value $30-60\%$: Perform a low-technology exercise test. A stair-climb height above $22\text{ m}$ or a shuttle-walk distance above $400\text{ m}$ indicates low risk; poorer performance requires CPET.
  • Either value $< 30\%$: Proceed directly to CPET.
• CPET Interpretation ($\dot{V}\text{O}_{2\text{peak}}$):
  • $> 20\text{ mL/kg/min}$ (or $>75\%$ predicted): Low risk; acceptable for anatomical resection, including pneumonectomy.
  • $10\text{ to }20\text{ mL/kg/min}$ (or $35\text{--}75\%$ predicted): Moderate risk; decisions depend on the extent of resection, and sublobar resection may be preferred.
  • $< 10\text{ mL/kg/min}$ (or $<35\%$ predicted): High risk, with mortality that may exceed $10\%$; minimally invasive or sublobar surgery, or non-surgical options such as stereotactic body radiotherapy (SBRT), should be discussed.
• ERS/ESTS 2009 (European): Measure FEV1 and DLCO in all candidates; if either is below $80\%$ predicted, perform CPET early in the assessment, then use the $\dot{V}\text{O}_{2\text{peak}}$ and predicted postoperative values to decide the safe extent of resection.

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2. One-Lung Ventilation (OLV): Indications and Isolation Devices

One-lung ventilation is the deliberate mechanical separation of the two lungs to isolate one lung or provide surgical exposure.

Devices for Lung Isolation: DLTs vs Bronchial Blockers

          [ Left-Sided DLT ]                       [ Right-Sided DLT ]

                 Trachea                                  Trachea
                    |                                        |
             Tracheal Lumen                           Tracheal Lumen
                    |                                        |
           Tracheal Cuff (Clear)                    Tracheal Cuff (Clear)
                    |                                        |
                 Carina                                   Carina
                /      \                                 /      \
      Right Main        Left Main              Right Main        Left Main
       Bronchus          Bronchus               Bronchus          Bronchus
                            |                       |     \
                     Bronchial Lumen         Bronchial    Right Upper
                            |                  Cuff       Lobe Orifice
                     Bronchial Cuff          (Features    (Aligned with
                         (Blue)               Slotted     Murphy Eye)
                                            Murphy Eye)

1. Double-Lumen Endobronchial Tubes (DLTs):
   • Left-Sided DLT (Standard): Used in over 95% of thoracic surgeries, including right-sided thoracotomies and resections. The left main bronchus is long (~4.5 to 5.0 cm) from carina to left upper lobe (LUL) takeoff, providing a wide margin of safety to seat the bronchial cuff without obstructing the LUL orifice.
   • Right-Sided DLT: Utilized primarily when a left-sided DLT is contraindicated (e.g. left pneumonectomy, left mainstem bronchial disruption, or left endobronchial tumour). Anatomical Challenge: The right upper lobe bronchus emerges only 1.5 to 2.0 cm from the carina. A right DLT must incorporate an asymmetric, slotted bronchial cuff with an opening (Murphy eye) that must align with microscopic precision opposite the RUL orifice. Misalignment by as little as 5 to 10 mm occludes RUL ventilation, triggering immediate severe hypoxemia and RUL atelectasis.
   • Confirmation of Position: Flexible fiberoptic bronchoscopy (FOB) is the gold standard:
     1. Tracheal inspection: Advance bronchoscope down the tracheal lumen. Confirm the carina is sharp, and the superior edge of the blue bronchial cuff is visible just distal to the carina inside the target bronchus, without herniating across the carina.
     2. Bronchial inspection: Advance bronchoscope down the bronchial lumen. For a left DLT, visualize the bronchial carina dividing into left upper and lower lobes. For a right DLT, inspect through the Murphy eye to confirm direct visualization of the RUL trifurcation (apical, anterior, posterior branches).
   • Cuff Pressures: Tracheal cuff (high volume, low pressure) inflated with 5-10 mL air; bronchial cuff (low volume, high pressure) inflated with only 1-3 mL air. Bronchial cuff pressure must remain $<20\text{ to }25\text{ cmH}_2\text{O}$ to prevent ischemic mucosal pressure necrosis, ulceration, or bronchial rupture.
2. Bronchial Blockers (e.g. Arndt, Cohen, Fuji, Univent):
   • Single-lumen endotracheal tube through which a catheter with an inflatable balloon tip is steered into a mainstem or lobar bronchus.
   • Key Indications: Known difficult airway (avoiding traumatic DLT exchange); existing tracheostomy; paediatric patients (smallest DLT is 26 Fr, suitable only for children $>8-10$ years); patients requiring postoperative mechanical ventilation (eliminates the need to exchange a DLT for an ETT at case conclusion); selective lobar isolation.

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3. Physiology of One-Lung Ventilation: Shunt and Hypoxic Vasoconstriction

Initiation of OLV in the lateral decubitus position redistributes pulmonary ventilation and perfusion, creating an obligate right-to-left transpulmonary shunt.

Blood Flow Redistribution and Transpulmonary Shunt

In the awake, upright individual, blood flow is distributed roughly 55% to the right lung and 45% to the left lung. In the anesthetized patient in the lateral decubitus position during two-lung ventilation:

• Dependent lung receives ~60% of total cardiac output (gravity-assisted perfusion).
• Non-dependent (operative) lung receives ~40% of total cardiac output.

When OLV is initiated, ventilation to the non-dependent lung ceases entirely ($V=0$), yet blood flow continues ($Q>0$). This non-dependent perfusion constitutes an obligatory right-to-left intrapulmonary shunt ($\dot{V}/\dot{Q} = 0$), carrying deoxygenated mixed venous blood directly into the left atrium to mix with oxygenated pulmonary venous blood from the dependent lung, precipitously lowering systemic $P_a\text{O}_2$.

Hypoxic Pulmonary Vasoconstriction (HPV)

Hypoxic Pulmonary Vasoconstriction is an intrinsic physiological homeostatic response of the pulmonary vasculature. In response to regional alveolar hypoxia ($P_A\text{O}_2 < 60\text{ mmHg}$ in collapsed alveoli), pre-capillary pulmonary vascular smooth muscle cells contract:

• HPV increases local pulmonary vascular resistance (PVR) in the non-ventilated, non-dependent lung.
• This diverts blood flow away from the non-ventilated lung and redirects it toward the well-ventilated, oxygenated dependent lung.
• Physiological Efficacy: Effective HPV reduces blood flow to the collapsed lung by 40% to 50%, decreasing the transpulmonary shunt from ~40% down to approximately 20% to 25% of cardiac output.

Factors Inhibiting / Blunting HPV

Anaesthetic management can inadvertently cripple HPV, converting mild desaturation into catastrophic refractory hypoxemia:

• Volatile Anaesthetics: Halogenated agents (isoflurane, sevoflurane, desflurane) inhibit HPV in a dose-dependent fashion. At concentrations $<1.0\text{ MAC}$, HPV inhibition is clinically negligible; at concentrations $>1.0\text{ MAC}$, significant HPV attenuation occurs. Note: Intravenous anaesthetics (Propofol / TIVA) do NOT inhibit HPV.
• Vasodilators: Nitroglycerin, sodium nitroprusside, calcium channel blockers, phosphodiesterase-5 inhibitors, and hydralazine directly dilate the constricted pulmonary vasculature in the hypoxic lung, massively increasing shunt.
• Hypocapnia / Alkalosis: Decreases PVR globally, blunting localized HPV responses.
• Excessive Pulmonary Pressures: Both extreme hypotension and extreme pulmonary arterial hypertension override HPV.
• Hypothermia: Impairs vascular smooth muscle reactivity.

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4. Evidence-Based Stepwise Protocol for Hypoxemia During OLV

If arterial oxygen saturation drops ($Sp\text{O}_2 < 90\%$ or $P_a\text{O}_2 < 60\text{ mmHg}$) during OLV, the anaesthesiologist must execute a rigorous stepwise escalation protocol:

                  [ STEPWISE HYPOXEMIA RESCUE IN OLV ]
                                    |
   [ STEP 1 ] ---> Check FiO2 (increase to 1.0) & Verify Position with FOB
                   (Exclude DLT displacement, herniation, secretion plugging)
                                    |
   [ STEP 2 ] ---> Optimize Dependent Lung Ventilation
                   - Tidal volume: 5-6 mL/kg (protective)
                   - Apply PEEP: 5-10 cmH2O (recruit atelectatic alveoli)
                   - Caution: Excessive PEEP (>12) increases dependent PVR!
                                    |
   [ STEP 3 ] ---> Apply CPAP to Non-Ventilated (Operative) Lung
                   - Continuous O2 flow with 1-5 cmH2O CPAP
                   - Most effective intervention for shunt reduction
                                    |
   [ STEP 4 ] ---> Refractory Hypoxemia Protocol
                   - High-frequency low-volume ventilation to operative lung
                   - Intermittent two-lung ventilation (notify surgeon)
                   - Surgical clamping of operative branch of pulmonary artery

1. Step 1: Increase $F_i\text{O}_2$ to 1.0 and Confirm DLT Position with FOB:
   • Immediately advance $F_i\text{O}_2$ to 100% on the ventilator.
   • Pass the flexible bronchoscope down the tracheal and bronchial lumina. Surgical traction, lateral decubitus flexion, or table movement frequently displaces the tube tip or herniates the bronchial cuff across the carina, obstructing the dependent mainstem bronchus.
   • Suction secretions and blood clots from the dependent tracheobronchial tree.
2. Step 2: Optimize Ventilation to the Dependent Lung:
   • Apply lung-protective mechanical ventilation: tidal volumes 5 to 6 mL/kg ideal body weight (IBW) to prevent barotrauma and volutrauma.
   • Apply 5 to 10 $\text{cmH}_2\text{O}$ of PEEP to recruit dependent atelectatic lung units, increasing functional residual capacity (FRC) above closing capacity.
   • Clinical Trap: Excessive PEEP ($>10-12\text{ cmH}_2\text{O}$) over-distends dependent alveoli, compresses pulmonary capillary networks, elevates dependent PVR, and paradoxically forces blood back into the non-ventilated operative lung, worsening the shunt!
3. Step 3: Apply Continuous Positive Airway Pressure (CPAP) to the Non-Dependent Lung:
   • Apply 1 to 5 $\text{cmH}_2\text{O}$ of CPAP with 100% $O_2$ to the non-ventilated operative lung.
   • Mechanism: Delivering a low positive pressure of pure oxygen maintains patency of non-ventilated alveoli without fully expanding the lung or compromising the surgical view. Blood traversing these un-collapsed capillaries becomes fully oxygenated, dramatically reducing the transpulmonary shunt.
4. Step 4: Refractory Hypoxemia Management:
   • Instruct the surgical team to halt resection temporarily and resume intermittent two-lung ventilation until oxygenation normalizes.
   • In cases of unilateral pneumonectomy, request immediate surgical clamping of the pulmonary artery branch supplying the diseased lung. Clamping instantly eliminates blood flow to the non-ventilated lung, converting the transpulmonary shunt into alveolar dead space and immediately curing the hypoxemia.

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5. Major Vascular Surgery: Abdominal Aortic Aneurysm (AAA) and Aortic Cross-Clamping

Aortic cross-clamping is required during open abdominal aortic aneurysm (AAA) repair and aortobifemoral bypass. The level of the aortic clamp (infrarenal, suprarenal, or supraceliac) dictates the severity of hemodynamic and metabolic derangements.

Hemodynamics of Aortic Cross-Clamping

Application of the cross-clamp creates an abrupt mechanical obstruction to blood flow:

• Increased Left Ventricular Afterload: Clamping causes a sudden, massive increase in Systemic Vascular Resistance (SVR) and total arterial elastance. Systolic arterial pressure and mean arterial pressure (MAP) above the clamp rise sharply.
• Preload Redistribution: Blood volume residing below the clamp is rapidly shifted toward the central and splanchnic venous capacitance reservoirs. Left ventricular end-diastolic volume (LVEDV), pulmonary capillary wedge pressure (PCWP), and LV wall stress increase substantially.
• Myocardial Strain and Ischemia: Increased afterload and wall tension drastically elevate myocardial oxygen demand ($M\dot{V}\text{O}_2$). If coronary reserves are marginal, subendocardial ischemia, acute LV dilation, and wall motion abnormalities develop. Vasodilators (nitroglycerin, nicardipine, clevidipine) or volatile depth titration are titrated to preserve cardiac output.
• Distal Ischemia: Complete cessation of blood flow below the clamp induces profound tissue ischemia in the lower extremities, pelvic viscera, and spinal cord. Suprarenal clamping additionally arrests renal blood flow, triggering acute tubular necrosis.

Hemodynamics of Aortic Unclamping ("Unclamping Shock")

Release of the aortic cross-clamp constitutes one of the most hazardous transitions in vascular anaesthesia:

• Sudden Drop in SVR: The re-opened distal vascular tree is maximally vasodilated secondary to accumulated local tissue hypoxia and ischemic paralysis of vascular smooth muscle tone. SVR plunges precipitously.
• Central Hypovolemia and Venous Pooling: Large volumes of circulating blood rush into the re-perfused distal capacitance vessels, causing severe central hypovolemia and sharp drops in CVP, PCWP, and venous return.
• Metabolic Washout: Perfusion of the ischemic lower extremities flushes massive quantities of toxic anaerobic metabolites into the systemic circulation:
  • Lactic acid and hydrogen ions ($H^+$) $\rightarrow$ severe metabolic acidosis.
  • Potassium ($K^+$) $\rightarrow$ acute hyperkalemia and risk of malignant ventricular arrhythmias.
  • Adenosine, prostaglandins, and Myocardial Depressant Factor (MDF) $\rightarrow$ acute negative inotropic depression and cardiac arrest.

Strategies to Prevent and Treat Unclamping Shock

1. Pre-emptive Volume Loading: In the 15 to 30 minutes prior to clamp release, administer crystalloids, colloids, or autologous blood from cell salvage to achieve high-normal filling pressures (CVP 10-12 mmHg, stroke volume variation $<10\%$).
2. Discontinue Vasodilators and Wean Volatiles: Stop all hypotensive infusions and lighten inhalational anaesthetic depth to baseline.
3. Prophylactic Vasopressor Support: Administer a prophylactic bolus or continuous infusion of norepinephrine or phenylephrine immediately prior to release.
4. Gradual and Controlled Clamp Release: Communicate with the surgeon to release the clamp slowly and incrementally (e.g. unclamping one iliac vessel first, observing the hemodynamic response for 2-3 minutes, then releasing the second).
5. Metabolic Correction: Administer Sodium Bicarbonate (50-100 mmol) to buffer metabolic acidosis, and Calcium Chloride (0.5-1.0 g) to stabilize the cardiac membrane against hyperkalemic arrest and bolster contractility.

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6. Thoracoabdominal Aortic Aneurysm (TAAA) Repair and Spinal Cord Protection

Repair of descending thoracic and thoracoabdominal aortic aneurysms (Crawford Extent I through IV) carries an ominous risk of ischemic spinal cord injury, presenting as postoperative paraplegia or anterior spinal artery syndrome (loss of bilateral motor function and pain/temperature sensation with preserved dorsal column vibration/proprioception).

       [ SPINAL CORD VASCULAR ARCHITECTURE & PERFUSION ]

                 Vertebral Arteries
                         |
             [ Anterior Spinal Artery (ASA) ]
           (Supplies Anterior 2/3 of Spinal Cord)
                         ^
                         |
          [ Artery of Adamkiewicz (T9-T12) ] <--- Left Intercostal Artery
          (Arteria Radicularis Magna)

       Spinal Cord Perfusion Pressure (SCPP) Formula:
       ---------------------------------------------
              SCPP = MAP - CSFP  (or CVP)

       Protection Targets: MAP >= 80-90 mmHg | CSFP < 10 mmHg

Spinal Cord Vascular Anatomy

• The anterior two-thirds of the spinal cord (containing the anterior motor horns and lateral corticospinal tracts) is supplied by the single, longitudinally oriented Anterior Spinal Artery (ASA).
• The ASA receives discontinuous radicular arterial inputs along its length. The largest and most critical radicular contributor is the Artery of Adamkiewicz (arteria radicularis magna), which originates from a left posterior intercostal or lumbar artery between T9 and T12 in over 75% of individuals (and between T8 and L2 in 95%). Cross-clamping or surgical ligation of these intercostal branches during TAAA resection abruptly arrests spinal cord perfusion.

Spinal Cord Protection Bundle

Spinal cord perfusion pressure (SCPP) is defined as: $SCPP = MAP_{\text{distal}} - CSFP \quad (\text{or } MAP - CVP, \text{whichever is higher})$ where $MAP_{\text{distal}}$ is the mean arterial pressure distal to the aortic cross-clamp, and $CSFP$ is the cerebrospinal fluid pressure.

1. Cerebrospinal Fluid (CSF) Drainage: A lumbar intrathecal drain is inserted preoperatively at L3-L4 or L4-L5. CSF is drained continuously or intermittently to maintain $CSFP < 10\text{ mmHg}$ (or $<8-10\text{ cmH}_2\text{O}$). This lowers the outflow resistance of the spinal venous and capillary beds, directly maximizing SCPP.
2. Distal Aortic Perfusion via Left Heart Bypass (LHB): Utilizes a centrifugal pump draining oxygenated blood from the left atrium (or left superior pulmonary vein) and pumping it directly into the left femoral artery or distal descending aorta. Maintains distal $MAP \ge 60\text{--}70\text{ mmHg}$, perfusing the kidneys, mesenteric bed, and lower intercostal arteries during cross-clamping, typically with heparin-bonded circuits and only low-dose systemic heparin rather than the full anticoagulation needed for cardiopulmonary bypass.
3. Moderate Systemic Hypothermia: Passive or active cooling to 32°C to 34°C reduces spinal cord neuronal metabolic oxygen demand.
4. Neurophysiological Monitoring:
   • Motor Evoked Potentials (MEPs): Evaluates descending motor tracts supplied by the anterior spinal artery. Loss of MEP amplitude $>50\%$ provides immediate, real-time warning of spinal cord ischemia within minutes of clamping.
   • Somatosensory Evoked Potentials (SSEPs): Evaluates dorsal columns supplied by the dual posterior spinal arteries. Less sensitive to anterior ischemia, as posterior perfusion may remain intact while anterior motor neurons undergo infarction.
   • Anaesthetic Constraint: Inhalational agents and neuromuscular blocking drugs severely suppress MEP signals; a Total Intravenous Anaesthesia (TIVA) regimen with propofol, remifentanil, and zero neuromuscular block (after intubation) is mandatory.
5. Intercostal Vessel Re-implantation: Critical intercostal arteries between T8 and L2 are re-implanted as a Carrel patch into the aortic vascular graft.

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7. Carotid Endarterectomy (CEA): Monitoring and Hemodynamics

Carotid endarterectomy involves surgical incision and plaque debridement of the common and internal carotid arteries to prevent ischemic stroke.

Neurological Monitoring Modalities

During internal carotid artery cross-clamping, cerebral perfusion to the ipsilateral hemisphere depends on collateral flow across the Circle of Willis via the anterior communicating and posterior communicating arteries.

1. Awake Patient under Regional Anaesthesia (Gold Standard):
   • Performed under superficial, intermediate, or deep cervical plexus block (targeting C2, C3, and C4 dermatomes) or local infiltration.
   • Continuous clinical assessment of consciousness, speech fluency (patient continuously counts or speaks), and contralateral motor function (patient regularly squeezes a squeaky toy in the contralateral hand). This provides immediate, unmistakable detection of cerebral ischemia, guiding selective placement of a temporary intraluminal shunt.
2. General Anaesthesia Monitoring:
   • Continuous Electroencephalography (EEG): Detects loss of high-frequency beta/alpha rhythms and appearance of high-amplitude delta slowing, indicating ischemia.
   • Near-Infrared Spectroscopy (NIRS / Cerebral Oximetry): Measures regional cerebral oxygen saturation ($rS\text{O}_2$) in frontal lobes. A drop of $>20\%$ from baseline indicates significant cerebral hypoperfusion warranting temporary shunting.
   • Carotid Artery Stump Pressure: Mean back-pressure measured in the cross-clamped internal carotid artery. A mean stump pressure $<40\text{ to }50\text{ mmHg}$ indicates inadequate collateral Circle of Willis flow, requiring immediate intraluminal shunt insertion.

Blood Pressure Titration and Postoperative Emergencies

• During Carotid Cross-Clamping: Maintain MAP at baseline to 10-20% above baseline (using phenylephrine or norepinephrine) to maximize collateral perfusion.
• Post-Endarterectomy / Unclamping: Strict blood pressure control is mandatory. Maintain systolic blood pressure $<140\text{ mmHg}$ (using short-acting IV labetalol, nicardipine, or clevidipine).
• Cerebral Hyperperfusion Syndrome (CHS): Occurs in 1% to 3% of patients following successful revascularization of high-grade, chronically stenotic lesions. Chronic hypoperfusion causes maximal autoregulatory vasodilation; when high-pressure arterial flow is suddenly restored, the paralyzed cerebral autoregulatory bed cannot constrict. Presents 2 to 7 days postoperatively with severe ipsilateral pounding headache, focal seizures, cerebral edema, and catastrophic intracerebral haemorrhage.
• Postoperative Neck Hematoma: Expanding wound hematoma compresses the anterior trachea and impedes cervical venous return, causing massive supraglottic laryngeal edema. Life-Saving Action: If airway compromise develops, the anaesthesiologist and surgical team must immediately open the surgical wound bedside, remove the skin clips/sutures, and evacuate the tension hematoma to decompress the airway prior to attempting tracheal reintubation.