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Lung Transplantation

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Abstract

Preoperative evaluation of the lung transplant recipient allows for optimal planning of intraoperative ventilation, hemodynamic support, and the need for extracorporeal support. Careful induction of anesthesia is required to avoid acute right ventricular failure and cardiovascular collapse, and transesophageal echocardiography is invaluable in the diagnosis of hemodynamic instability. The increasing perioperative use of extracorporeal membrane oxygenation bestows new challenges on the anesthesiologist, in terms of hemodynamic, anticoagulation, and fluid management. Early postoperative extubation is feasible, and reduction in early complications confers a long-term survival benefit.

Keywords

  • Donor organ
  • End-stage lung disease
  • Extracorporeal support
  • Lung transplantation
  • Right ventricular failure

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Clinical Case Discussion

Clinical Case Discussion

Case Presentation

A 52-year-old male with mixed interstitial lung disease/COPD presents for right single-lung transplantation via right thoracotomy and left hemidiaphragm plication. He requires supplemental oxygen at 3 lpm at rest and 10 lpm with exertion. He has a 40-pack-year smoking history and quit 5 years ago. His history is notable for five-vessel coronary artery bypass graft 8 years ago and endovascular repair of an abdominal aortic aneurysm 5 years ago. As a teenager, he suffered a traumatic injury to his left neck, resulting in left vocal cord and hemidiaphragm paralysis.

His preoperative medication list includes albuterol, atorvastatin, azithromycin, gabapentin, metoprolol, omeprazole, sertraline, and sildenafil. He has no medication allergies.

The patient’s preoperative workup reveals the following information:

  • Weight: 87 kg, Height: 176 cm, Heart rate: 80 bpm, Blood pressure: 108/70 mmHg Temperature: 37.0 °C, SpO2: 97% on 3 L nasal cannulae

  • ECG: normal sinus rhythm with occasional premature ventricular contractions, left ventricular hypertrophy

  • Hemoglobin: 13.7 g/dL, hematocrit: 42.3%, white blood cell count: 10 x109/L, platelets 229 × 109/L

  • Na+: 138 mmol/L, K+: 4.1 mmol/L, Cl-: 103 mmol/L, CO2: 28 mmol/L, BUN 20 mg/dL, Cr 0.8 mg/dL, Glucose 103 mg/dL, INR 1.0

  • Arterial blood gas on room air: pH 7.37, pCO2 49 mmHg, pO2 59 mmHg, bicarbonate 28 mmol/L, base excess 2 mmol/L

  • FEV1 51% predicted, FVC 59% predicted, FEV1/FVC 86

  • Ventilation/perfusion scan: differential perfusion is 46% to left lung, 54% to right lung

  • Transthoracic echocardiogram: left ventricular ejection fraction 50% with inferior hypokinesis, normal right ventricular systolic function, trivial tricuspid regurgitation

  • Left heart catheterization: significant native vessel coronary artery disease, all grafts patent

  • Right heart catheterization: pulmonary artery (PA) pressure 52/14 mmHg (mean 28), pulmonary vascular resistance 2.4 Wood units, cardiac index 2.6 L/min-m2, pulmonary capillary wedge pressure 9 mmHg

  • Preoperative imaging studies are shown in Figs. 47.7 and 47.8.

Fig. 47.7
figure 7

Preoperative upright posterior-anterior chest X-ray. Notable findings include left hemidiaphragm elevation, changes consistent with post median sternotomy and CABG, and aortic stent graft within the abdomen

Fig. 47.8
figure 8

Coronal slice from preoperative computed tomography (CT) scan of the chest. Notable findings are left hemidiaphragm elevation with volume loss in the left hemithorax, right lung hyperinflation, and paraseptal emphysema in the bilateral lung apices

Questions

  1. 1.

    Would you insert a central line and/or pulmonary artery catheter prior to the induction of anesthesia? Does the laterality of central line insertion matter?

  2. 2.

    How would you induce anesthesia in this patient?

  3. 3.

    How would you secure the airway?

  4. 4.

    How would your anesthetic considerations differ if the patient had:

    1. (a)

      Cystic fibrosis?

    2. (b)

      COPD?

    3. (c)

      Primary pulmonary hypertension?

  5. 5.

    Can this transplant be done without cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO)?

Case Continuation

After the induction of anesthesia, intubation with a left-sided double-lumen tube, and insertion of all invasive monitors and a TEE probe, lung isolation is achieved, and one-lung ventilation (OLV) is established. After 30 min of dissection and OLV, the patient remains hemodynamically stable, but the SpO2 has decreased to 85% on 100% inspired oxygen, and the arterial blood gas now reads pH 7.21, pCO2 68 mmHg, pO2 51 mmHg, bicarbonate 22 mmol/L, and base excess −2 mmol/L.

Questions

  1. 6.

    How will you manage OLV?

  2. 7.

    How will you address the hypoxemia that has developed during OLV? What degree of hypoxemia and/or hypercarbia will you tolerate?

Case Continuation

In preparation for explant of the native right lung, the surgeon clamps the right PA. After clamping, the vitals are heart rate 90 bpm, blood pressure 129/74 mmHg, central venous pressure 10 mmHg, PA pressure 46/17 (mean 29) mmHg, and SpO2 99%.

The right lung is explanted. Then the right donor lung is implanted and reperfused, during which time there is severe hemodynamic instability.

Questions

  1. 8.

    How would you expect pulmonary arterial pressures to change with clamping of the left PA?

  2. 9.

    What has caused the hemodynamic instability?

Case Continuation

The donor (right) lung is now ventilated. Soon after, frank pulmonary edema is seen coming from the tracheal (right) lumen of the double-lumen tube.

Questions

  1. 10.

    How would you ventilate the donor lung?

  2. 11.

    Transesophageal echocardiography pulse-wave Doppler evaluation of the right pulmonary veins reveals a peak velocity of 110 cm/s. How would you advise the surgeon?

  3. 12.

    What is the reason for the development of pulmonary edema?

Discussion

  • Question 1: Would you insert a central line and/or pulmonary artery catheter prior to the induction of anesthesia? Does the laterality of central line insertion matter?

This patient does not have significant pulmonary hypertension; thus, the preinduction insertion of a pulmonary artery catheter (PAC) is not required. However, in a patient with significant pulmonary hypertension, the preinduction insertion of a PAC allows for precise hemodynamic management during induction of anesthesia. Central access also offers the advantage of allowing for the use of inotrope infusions (e.g., epinephrine) to support the right ventricle, although this central access is not necessarily required for temporary infusions. Of note, many lung transplant patients will not be able to tolerate preinduction central line/PAC insertion because they may not tolerate Trendelenburg or even supine positioning. Importantly, extreme caution must be taken in administering sedation to lung transplant recipients who often have tenuous respiratory status. The potential exacerbation of baseline hypercapnia or hypoxemia with sedation may precipitate an acute increase in pulmonary vascular resistance and subsequent right ventricular dysfunction/failure with cardiovascular collapse.

If the patient’s pulmonary arterial pressures are approaching or even supra-systemic, it may be prudent to consider preinduction cannulation of the femoral vessels under local anesthesia for either preemptive or emergent institution of ECMO/CPB. Our practice is to typically place the central line and PAC via the left internal jugular vein under ultrasound guidance; this leaves the right internal jugular vein accessible should circulatory support (e.g., ECMO) be required during or after the transplant procedure. In this patient, vascular access in the left neck may be complicated by his previous injury.

  • Question 2: How would you induce anesthesia in this patient?

The induction of anesthesia in lung transplant recipients should focus on extreme attention to hemodynamic stability and management of pulmonary hypertension as well as rapid securement of the airway. With regard to the management of pulmonary hypertension, it is paramount to avoid significant decreases in systemic vascular resistance that will reduce right ventricular perfusion, thus compromising RV function. One must also limit any increase in pulmonary vascular resistance by avoiding hypoxemia, hypercarbia, acidosis, and “light” anesthesia during laryngoscopy and intubation. A preinduction arterial catheter is mandatory for beat-to-beat blood pressure monitoring, and a cardiac-style induction relying primarily on narcotics and benzodiazepines often provides the desired hemodynamic stability. Although rapid securement of the airway is desirable, conventional rapid sequence induction techniques may not be tolerated in patients with RV dysfunction. Despite the potential for adrenocortical suppression, some practitioners select etomidate as part of a rapid sequence induction in combination with succinylcholine. Regardless of the drugs selected for induction, vasoconstrictors and inotropes should be readily available for hemodynamic support and resuscitation. Inotropes without systemic vasodilatory effects are preferred. Careful preoperative assessment of the airway and contingency planning for difficult airway access are prudent, as these patients may not tolerate prolonged periods of apnea. Given the left hemidiaphragm paralysis in this patient, with resultant low lung volumes on the left, this patient may experience more rapid desaturation during induction than might be predicted from his lung disease. Furthermore, this patient is only undergoing single-lung transplantation; therefore, precautions against aspiration, which could compromise the remaining native lung, should be taken.

  • Question 3: How would you secure the airway?

In the vast majority of lung transplant patients, a left-sided double-lumen endotracheal tube (ETT) placed with bronchoscopic guidance is typically used. Patients with a suppurative pathology (e.g., cystic fibrosis) will benefit from initial insertion of a single-lumen ETT to allow for pulmonary toilet via bronchoscopy. This will mostly likely improve oxygenation during one-lung ventilation.

Bronchial blockers to achieve lung isolation are more prone to movement within the airway during manipulation of the hilum and do not allow for effective suctioning, the application of continuous positive airway pressure (CPAP) to the non-ventilated lung, or differential ventilation of the two lungs.

  • Question 4: How would your anesthetic considerations differ if the patient had:

    1. (a)

      Cystic fibrosis?

    2. (b)

      COPD?

    3. (c)

      Primary pulmonary hypertension?

The leading indications for lung transplantation today are pulmonary fibrosis, COPD, and cystic fibrosis. The underlying pathology impacts the surgical procedure as well as the anesthetic considerations. For example, patients with fibrosis often receive single-lung transplants, while patients with cystic fibrosis always require a double-lung transplant.

Induction techniques are similar for all pathologies and reflect consideration of pulmonary artery pressures and underlying right ventricular function, as described above.

Ventilation strategies, on the other hand, should be tailored to the underlying pulmonary pathology. Patients with pulmonary fibrosis have low lung compliance and are at risk for barotrauma associated with mechanical ventilation. Pressure control ventilation may be preferable to volume control ventilation to decrease the airway pressure transmitted to the lungs. Patients with obstructive lung disease, such as COPD or cystic fibrosis, are prone to air trapping and dynamic hyperinflation (see question 6).

Patients such as this one who receive single-lung transplants may have a significant imbalance in pulmonary compliance between the native lung and the transplanted lung, requiring differential lung ventilation via a double-lumen ETT.

  • Question 5: Can this transplant be done without cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO)?

Cardiopulmonary bypass (CPB) offers the advantage of improved hemodynamic stability and systemic oxygenation during lung transplantation. However, CPB has many disadvantages, including bleeding related to full heparinization and coagulopathy, increased use of blood products, increased crystalloid administration, inflammation, and possible damage to other organs. Nonetheless, patients with intractable hypoxemia during one-lung ventilation or RV dysfunction causing hemodynamic compromise may require ECMO or CPB to safely complete the procedure. ECMO is often preferred over CPB because it allows for less heparinization and can be easily extended into the postoperative period if required.

  • Question 6: How will you manage OLV?

Concerns during OLV before transplant include hypoxemia, hypercarbia, dynamic hyperinflation (in cases of obstructive lung disease), and excessively high airway pressures (which may precipitate RV failure). To address dynamic hyperinflation, ventilation should focus on permissive hypercapnia with reduced tidal volume, lower respiratory rate, elimination of positive end-expiratory pressure (PEEP), and adjustments to inspiratory/expiratory (I:E) ratio to favor exhalation. Elevated airway pressures can be ameliorated through reduced tidal volumes, higher respiratory rate, and adjustment of the ventilator I:E ratio.

  • Question 7: How will you address the hypoxemia that has developed during OLV? What degree of hypoxemia and/or hypercarbia will you tolerate?

Hypoxemia during one-lung ventilation (OLV) can be treated with either continuous positive airway pressure (5–10 cmH2O) to the non-ventilated lung to oxygenate the shunt fraction or with PEEP (5–10 cmH2O) to the ventilated lung to minimize atelectasis. Of note, PEEP can potentially reduce venous return to the heart, impair hypoxic pulmonary vasoconstriction, and elevate pulmonary vascular resistance. Definitive treatment of hypoxemia due to shunt during OLV is achieved with surgical clamping of the PA to the non-ventilated lung. Hypoxic pulmonary vasoconstriction may be improved by reducing inhaled volatile anesthetic concentration or utilizing TIVA only and by avoiding IV vasodilators (e.g., nitroglycerin). If intractable hypoxemia occurs despite the above maneuvers and utilization of 100% inspired oxygen, ECMO or CPB may be required.

Management of arterial blood gas values should target the patient’s baseline values prior to induction of anesthesia. While some degree of permissive hypercarbia may be necessary to achieve adequate oxygenation, severe hypercarbia, hypoxemia, or acidosis that produce hemodynamic instability are indications for ECMO or CBP.

  • Question 8: How would you expect pulmonary arterial pressures to change with clamping of the left PA?

It is reasonable to expect a rise in the PA pressure after surgical clamping of either pulmonary artery because the entire cardiac output is now passing through the contralateral lung. This PA pressure increase may be variable depending on the degree of baseline perfusion through the native lung (reference the preoperative ventilation/perfusion lung scan). While a lack of increase in PA pressure with PA clamping may seem reassuring, the anesthesiologist should always be vigilant about the possibility of worsening of RV function.

  • Question 9: What has caused the hemodynamic instability?

Possible causes of hemodynamic instability in this scenario include worsening of RV function, worsening of LV function due to ischemia in this patient with significant coronary disease, and air embolism occurring during reperfusion of the transplanted lung. The best tool for monitoring cardiac function and for diagnosing the cause of intraoperative hemodynamic instability is transesophageal echocardiography (TEE). TEE will be able to differentiate between these scenarios and allow for determination of the cause of hemodynamic instability.

  • Question 10: How would you ventilate the donor lung?

Goals for the management of any newly transplanted lung include the avoidance of atelectasis, hyperoxia, and barotrauma, which can rapidly cause pulmonary edema. During double-lung transplantation, a particularly vulnerable period occurs between the first and second implant when the newly reperfused first lung must tolerate twice the normal blood flow (i.e., the full cardiac output). Single-lung transplants are vulnerable to differences in compliance between the newly implanted lung and the remaining native lung. Institutional perioperative standardized practices for ventilation of the newly transplanted lung are common for goal PEEP (e.g., 8 mmHg), preferred oxygen levels (e.g., room air or the lowest inspired oxygen concentration to maintain SpO2 above 90%), and peak inspiratory pressure (e.g., less than 30 mmHg). At our institution, inhaled nitric oxide (iNO) or inhaled epoprostenol are routinely administered to reduce pulmonary artery pressure and support RV function, although the benefits in lung transplantation are controversial.

  • Question 11: TEE pulse-wave Doppler evaluation of the R pulmonary veins reveals a peak velocity of 110 cm/s. How would you advise the surgeon?

Pre-procedure and post-procedure TEE evaluation provides invaluable information to assist with anesthetic management and to aide in diagnosing surgical complications. Pre-procedure evaluation should focus on RV and LV function, the identification and quantification of any valvular lesions or intracardiac shunts (e.g., PFO), and an assessment of baseline pulmonary vein velocities and pulmonary artery size.

Post-transplant TEE should again evaluate RV and LV function. Most importantly, following reperfusion there should be a careful assessment of the right and left pulmonary arteries and all four pulmonary veins (if possible), including:

  • Assessment of the diameter of pulmonary artery and pulmonary vein anastomoses, if visible

  • Color flow Doppler evaluation of pulmonary artery anastomoses, if visible

  • Color flow Doppler evaluation of pulmonary vein flows and pulsed-wave Doppler determination of pulmonary vein velocities

In general, anastomoses >0.5 cm in diameter and pulmonary vein pulse-wave Doppler peak systolic velocities ≤100 cm/s are acceptable. Although few specific guidelines exist, peak systolic velocities >100–170 cm/s are worrisome for obstruction (kinked or narrow anastomoses) and should prompt discussion with the surgical team before chest closure.

  • Question 12: What is the reason for the development of pulmonary edema?

Reperfusion injury typically presents with poor oxygenation, high PA pressures, and pulmonary edema. It is important to exclude a mechanical cause, such as pulmonary vein or arterial anastomotic stenosis or kinking (best evaluated via TEE, as described above). Otherwise, protective lung ventilation strategies should be employed. Inhaled pulmonary vasodilators can help to reduce the inspired oxygen concentration in patients with high oxygen requirements. Ultimately, significant reperfusion injury or primary graft dysfunction may necessitate the use of ECMO.

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Roscoe, A., Klinger, R.Y. (2019). Lung Transplantation. In: Slinger, P. (eds) Principles and Practice of Anesthesia for Thoracic Surgery. Springer, Cham. https://doi.org/10.1007/978-3-030-00859-8_47

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