Thoracic Anesthesia during the COVID-19 Pandemic: 2021 Updated Recommendations by the European Association of Cardiothoracic Anaesthesiology and Intensive Care (EACTAIC) Thoracic Subspecialty Committee.

The novel coronavirus pandemic has radically changed the landscape of normal surgical practice. Lifesaving cancer surgery, however, remains a clinical priority, and there is an increasing need to fully define the optimal oncologic management of patients with varying stages of lung cancer, allowing prioritization of which thoracic procedures should be performed in the current era. Healthcare providers and managers should not ignore the risk of a bimodal peak of mortality in patients with lung cancer; an imminent spike due to mortality from acute coronavirus disease 2019 (COVID-19) infection, and a secondary peak reflecting an excess of cancer-related mortality among patients whose treatments were deemed less urgent, delayed, or cancelled. The European Association of Cardiothoracic Anaesthesiology and Intensive Care Thoracic Anesthesia Subspecialty group has considered these challenges and developed an updated set of expert recommendations concerning the infectious period, timing of surgery, vaccination, preoperative screening and evaluation, airway management, and ventilation of thoracic surgical patients during the COVID-19 pandemic.

Thoracic Anesthesia of Patients With Suspected or Confirmed 2019 Novel Coronavirus Infection: Preliminary Recommendations for Airway Management by the European Association of Cardiothoracic Anaesthesiology Thoracic Subspecialty Committee.

The novel coronavirus has caused a pandemic around the world. Management of patients with suspected or confirmed coronavirus infection who have to undergo thoracic surgery will be a challenge for the anesthesiologists. The thoracic subspecialty committee of European Association of Cardiothoracic Anaesthesiology (EACTA) has conducted a survey of opinion in order to create recommendations for the anesthetic approach to these challenging patients. It should be emphasized that both the management of the infected patient with COVID-19 and the self-protection of the anesthesia team constitute a complicated challenge. The text focuses therefore on both important topics.

Hypoxemia during one-lung ventilation: prediction, prevention, and treatment.

When switching from two-lung to one-lung ventilation (OLV), shunt fraction increases, oxygenation is impaired, and hypoxemia may occur. Hypoxemia during OLV may be predicted from measurements of lung function, distribution of perfusion between the lungs, whether the right or the left lung is ventilated, and whether the operation will be performed in the supine or in the lateral decubitus position. Hypoxemia during OLV may be prevented by applying a ventilation strategy that avoids alveolar collapse while minimally impairing perfusion of the dependent lung. Choice of anesthesia does not influence oxygenation during clinical OLV. Hypoxemia during OLV may be treated symptomatically by increasing inspired fraction of oxygen, by ventilating, or by using continuous positive airway pressure in the nonventilated lung. Hypoxemia during OLV may be treated causally by correcting the position of the double-lumen tube, clearing the main bronchi of the ventilated lung from secretions, and improving the ventilation strategy.

Oxygenation during one-lung ventilation with propofol or sevoflurane.

60 patients, ASA I-III, underwent one-lung ventilation for open or video-assisted thoracic surgery randomized either with intravenous anesthesia with propofol or with inhalational anesthesia with 1 MAC sevoflurane. Propofol was titrated during one-lung ventilation to achieve a mean arterial pressure of 75-80 mmHg. Blood gas analyses, hemodynamic and respiratory parameters were measured during two-lung ventilation at the beginning of the surgical procedure and 10 min, 20 min and 30 min after start of one-lung ventilation. At all time points, hemodynamic and respiratory parameters were comparable in both groups. Oxygenation did not differ between groups at comparable mean arterial blood pressures.

A novel model of selective lung ventilation to investigate the long-term effects of ventilation-induced lung injury.

Mechanical ventilation (MV) with large tidal volumes (V(T)) causes ventilator induced lung injury. Whereas immediate effects of short-term injurious ventilation are well studied, little is known about its long-term effects. We aimed to establish an animal model of selective injurious MV, permitting assessment of the long-term course of ventilation-induced lung injury. In anesthetized and instrumented rats (n = 26), laryngoscopy was performed, and one cannula for MV was placed in the left main bronchus and a second one in the trachea. Two ventilators were used to ventilate the left lung with high (20 mL/kg) and the right lung with low (4 mL/kg) V(T). In control animals, both lungs received low V(T). After 2 h of MV, animals were extubated and observed for 24 h and then killed. Left and right lungs were excised and sampled for further investigations. Survival in animals ventilated with the high V(T) was 90%. Twenty-four hours after MV, alveolar levels of humoral (tumor necrosis factor alpha, interleukin 6) and cellular (polymorphonuclear leukocytes) inflammatory markers were increased, and histological alterations were present in lungs ventilated with high V(T). A delayed decrease in PaO2 was noted 24 h after MV, with high V(T) delivered to one lung as compared with low V(T) delivered to both lungs. This animal model permits assessment of the long-term course of ventilation-induced lung injury and shows that pulmonary inflammation and histological alterations are present 24 h after unilateral injurious ventilation.

PEEP has beneficial effects on inflammation in the injured and no deleterious effects on the noninjured lung after unilateral lung acid instillation.

OBJECTIVE: In clinical lung injury areas of inflammation and structural alveolar alteration are unevenly distributed and interspaced between healthy or less injured lung areas. Positive end-expiratory pressure (PEEP) applied with mechanical ventilation (MV) may affect injured and healthy lung areas differently. We compared the effects of PEEP on the inflammatory response in injured and noninjured regions of the lung in an animal model of unilateral lung acid instillation. SUBJECTS: Anesthetized, paralyzed, and ventilated rats. INTERVENTIONS: Rats underwent left-endobronchial instillation with either hydrochloric acid or isotonic saline and were randomized 24 h later to MV using constant tidal volume (16 ml/kg) with either ZEEP, PEEP at 5 mmHg, or PEEP at 10 mmHg. After 4 h of MV the animals (n=9 or 10 per group) were killed and inflammatory markers assessed in left- and right-lung lavage fluid samples. In four additional animals per group differential lung perfusion was assessed. RESULTS: Unilateral acid injury alone worsened oxygenation, decreased left-lung perfusion, and increased left-lung lavage neutrophil and macrophage counts and cytokine levels. MV with ZEEP further impaired oxygenation and further decreased left-lung perfusion in acid-injured animals. MV with high PEEP preserved oxygenation and significantly decreased left-lung lavage protein content and cell counts in acid-injured animals and had no deleterious effect on the right (noninjured) lung. CONCLUSION: In this model of unilateral lung acid injury high PEEP attenuates the inflammatory cell response in the acid-injured lung, preserved oxygenation and has no deleterious effects in the opposite lung.

Percutaneous transtracheal ventilation: effects of a new oxygen flow modulator on oxygenation and ventilation in pigs compared with a hand triggered emergency jet injector.

The application of percutaneous transtracheal jet ventilation for emergency ventilation depends on special equipment which is often not available outside the operating room. The oxygen flow modulator is a new specially designed device for emergency ventilation using a low pressure oxygen supply. We studied the effects of the new device in comparison with a hand triggered emergency jet injector on oxygenation and ventilation in six pigs (21+/-1 kg). The animals were anaesthetized, tracheally intubated, and mechanically ventilated. Following central venous and pulmonary artery catheterization, a Paratrend 7 sensor was placed in the left femoral artery for continuous measurements of PaO(2) and PaCO(2). Then an emergency transtracheal airway catheter was inserted into the trachea after surgical exposure. In randomized order each animal was ventilated via the transtracheal airway catheter with the hand triggered emergency jet injector (inspiratory/expiratory (I/E) ratio of 1:1; respiratory rate of 60 min(-1); driving pressure 1.5 bar; FjetO(2) 1.0) and the oxygen flow modulator (FiO(2) 1.0 at an oxygen flow of 15 l min(-1); respiratory rate of 60 min(-1); I/E ratio of approximately 1:1) for 15 min each. After each phase of the experiment respiratory and hemodynamic variables were measured. Whereas PaO(2) was not significantly different between the two devices, PaCO(2) was higher during the hand-triggered jet ventilation. Thus, the efficacy of the oxygen flow modulator during the experiment was comparable with the efficacy of the hand triggered emergency jet injector.

Effects of a catecholamine-induced increase in cardiac output on lung injury after experimental unilateral pulmonary acid instillation.

OBJECTIVES: Increasing pulmonary blood flow aggravated ventilation-associated lung injury in ex vivo animal experiments, but data were less consistent in an in vivo animal model and do not reflect redistributed lung perfusion seen in clinical acute lung injury. We sought to determine the effects of increased cardiac output on markers of lung injury in an in vivo model of inhomogeneous lung perfusion and injury. DESIGN: Prospective, controlled animal study. SETTING: Experimental research laboratory of a university hospital. SUBJECTS: A total of 50 anesthetized, mechanically ventilated, male Wistar rats. INTERVENTIONS: Unilateral lung injury was induced in rats by left lung acid instillation. After 24 hrs, animals were anesthetized and subjected to mechanical ventilation (tidal volume, 8 mL/kg; positive end-expiratory pressure, 7 cm H2O; FIO2, 0.4) and continuous infusion of either 10 microg x kg x min dobutamine or isotonic saline (control) for 4 hrs. MEASUREMENTS AND MAIN RESULTS: Cardiac output and differential lung perfusion were recorded throughout the ventilation period. Right and left lung wet-to-dry weight ratio, cytokines and inflammatory cells in lung lavage, and histologic lung injury were measured postmortem. After acid injury, lung perfusion was preferentially distributed to the noninjured lung. Dobutamine increased baseline cardiac output (>70%) and perfusion of both lungs (left, acid-instilled lung: from 16 +/- 2 to 29 +/- 6 mL/min; right, non-acid-instilled lung: from 54 +/- 3 to 98 +/- 7 mL/min). There was no difference in left lung injury between dobutamine- and saline-infused animals, but right lung injury was aggravated in dobutamine-infused animals, as indicated by increased lung edema, histologic lung injury, and cell counts in lavage. CONCLUSIONS: In the setting of unilateral lung injury and uneven lung perfusion, a dobutamine-induced increase in cardiac output has potentially detrimental effects on the opposite lung.

Increased susceptibility to ventilator-associated lung injury persists after clinical recovery from experimental endotoxemia.

BACKGROUND: Endotoxin, when delivered shortly before or during mechanical ventilation, increases susceptibility to ventilation-associated lung injury. However, it is unclear whether increased susceptibility to ventilator-associated lung injury is still present after clinical recovery from a transient endotoxin challenge. METHODS: Anesthetized rats were submitted to a 4-h period of mechanical ventilation with low (8 ml/kg) or high (24, 27, or 30 ml/kg) tidal volumes (VTs) 24 h after transient illness had been provoked by a single nonlethal intravenous injection of Escherichia coli endotoxin. Control animals were injected with phosphate-buffered saline and underwent the same protocol. RESULTS: At 24 h, endotoxin-treated nonventilated animals showed no symptoms of clinical illness, and oxygenation was comparable with that of controls, but lung neutrophil counts were increased. Compared with controls, mechanical ventilation with high VT induced a stronger pulmonary inflammatory response and more severe lung injury in endotoxin-treated animals, as indicated by impaired oxygenation, increased lung wet-to-dry weight ratio, and increased levels of protein, neutrophils, and cytokines in lung lavage fluid. In addition, the highest VT resulted in increased mortality in endotoxin-treated animals. Low VT after endotoxin treatment did not cause functional pulmonary impairment but induced an inflammatory response. CONCLUSIONS: In this animal model, a 24-h delay after a single systemic injection of endotoxin resulted in clinical recovery and preserved pulmonary function but did not prevent increased susceptibility to ventilator-associated lung injury provoked by high VT. Residual pulmonary inflammation and neutrophilic infiltration at initiation of mechanical ventilation probably contribute to these findings.

Extravasation injury in the perioperative setting.

Extravasation is an unintentional injection or leakage of fluid in the perivascular or subcutaneous space. Extravasation injury results from a combination of factors, including solution cytotoxicity, osmolality, vasoconstrictor properties, infusion pressure, regional anatomical peculiarities, and other patient factors. We reviewed the hospital files of patients who had sustained a significant extravasation injury in the perioperative setting at two German hospitals. These cases highlight the risk of devastating consequences from extravasation injury. Vasoactive drugs and hyperosmolar and concentrated electrolyte solutions are the predominant vesicants in the perioperative setting. Prompt and appropriate intervention is important for avoiding or minimizing extensive tissue injury.

The effects of xenon or nitrous oxide supplementation on systemic oxygenation and pulmonary perfusion during one-lung ventilation in pigs.

During experimental one-lung ventilation (OLV), the type of anesthesia may alter systemic hemodynamics, lung perfusion, and oxygenation. We studied whether xenon (Xe) or nitrous oxide (N(2)O) added to propofol anesthesia would affect oxygenation, lung perfusion, and systemic and pulmonary hemodynamics during OLV in a pig model. Nine pigs were anesthetized, tracheally intubated, and mechanically ventilated. After placement of arterial and pulmonary artery catheters, a left-sided double-lumen tube was placed via tracheotomy. IV anesthesia with propofol was supplemented in random order with N(2)O/O(2) 60:40 or Xe/O(2) 60:40 or N(2)/O(2) 60:40. All measurements were made after stabilization at each concentration. Differential lung perfusion was measured with colored microspheres. Oxygenation (Pao(2): 90 +/- 17, 95 +/- 20, and 94 +/- 20 mm Hg for N(2)/O(2), N(2)O/O(2), and Xe/O(2)) and left lung perfusion (16% +/- 5%, 14% +/- 6%, and 18.8% for N(2)/O(2), N(2)O/O(2), and Xe/O(2)) during OLV did not differ among the 3 groups. However, mean arterial blood pressure (78 +/- 25, 62 +/- 23, and 66 +/- 23 mm Hg for N(2)/O(2), N(2)O/O(2), and Xe/O(2)) and mixed venous saturation (55% +/- 12%, 48% +/- 12%, and 50% +/- 12% for N(2)/O(2), N(2)O/O(2), and Xe/O(2)) were reduced during N(2)O/O(2) as compared with the control group (N(2)/O(2)). Supplementation of IV anesthesia with Xe or N(2)O does not impair oxygenation nor alter lung perfusion during experimental OLV.

Neutrophil stimulation with granulocyte colony-stimulating factor worsens ventilator-induced lung injury and mortality in rats.

BACKGROUND: Based on the association between the neutrophil and ventilator-induced lung injury, the authors hypothesized that neutrophil inhibition with fucoidin would be beneficial and stimulation with granulocyte colony-stimulating factor (G-CSF) would be harmful in a rat model of lethal ventilator-induced lung injury. METHODS: Animals (n = 111) were randomly assigned to be pretreated with fucoidin, G-CSF, or placebo (control) before 4 h of low-tidal-volume (10 ml/kg) or high-tidal-volume (40 ml/kg) mechanical ventilation. RESULTS: All low-volume animals survived. With high volumes, compared with controls, fucoidin did not improve survival (3 of 20 control animals and 5 of 20 fucoidin animals died; P = 0.51) but G-CSF significantly worsened it (18 of 22 animals died; P < 0.001). Circulating neutrophils were increased early with G-CSF and late with fucoidin with low and high tidal volumes (P < 0.05 for each treatment and tidal volume). Fucoidin decreased lung neutrophils, but these were only significant with high tidal volumes, whereas G-CSF increased lung neutrophils but only significantly with low tidal volumes (P < or = 0.01 for each). Fucoidin did not alter any cardiopulmonary measure significantly. Compared with control, G-CSF increased airway pressures with high tidal volumes and worsened lung edema and arterial oxygen with both tidal volumes (P < 0.05 for each). CONCLUSIONS: In this model, neutrophil stimulation by G-CSF increased lung dysfunction and with high tidal volumes worsened survival rates. Extrapolated clinically, neutrophil stimulation either by agents such as G-CSF or conditions such as sepsis may aggravate ventilator-induced lung injury.

The effects of urapidil on thermoregulatory thresholds in volunteers.

UNLABELLED: In a previous study we have shown that the antihypertensive drug, urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS: In this study we show that the antihypertensive drug urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.

Measuring cardiac output in one-lung ventilation: a comparison of pulmonary artery and transpulmonary aortic measurements in pigs.

OBJECTIVE: The agreement between cardiac output measurements via pulmonary artery thermodilution (CO[PA]) and transpulmonary aortic thermodilution (CO[AT]) during one-lung ventilation was studied. DESIGN: Animal study with repeated simultaneous measurements comparing 2 cardiac output measurement techniques. SETTING: Experimental animal facility of a university department. PARTICIPANTS: Forty-eight female pigs (26-42 kg). INTERVENTIONS: The pigs were anesthetized, tracheally intubated, and mechanically ventilated. After placement of an aortic thermistor catheter via the femoral artery and a pulmonary artery catheter, a double-lumen tube was placed via tracheotomy. During one-lung ventilation in each animal, 3 measurements with pulmonary artery thermodilution and transpulmonary aortic thermodilution were performed in different hemodynamic states. Both thermistors were connected to 1 computer system, and 144 simultaneous cardiac output measurements were analyzed. MEASUREMENTS AND MAIN RESULTS: Linear regression analyses revealed a close relationship between the 2 methods: CO(AT) = 0.81 CO(PA) + 1.04 (L/min) (r = 0.96, p < 0.0001). Bland-Altman analysis showed that CO(AT) was slightly higher than the CO(PA) with a bias of 0.2 +/- 0.5 L/min. However, in higher CO states, an inversion of this relationship was found, possibly because of indicator loss and recirculation. CONCLUSIONS: The pulmonary artery thermodilution and the transpulmonary aortic thermodilution techniques both accurately measure cardiac output during one-lung ventilation.

Lung perfusion, shunt fraction, and oxygenation during one-lung ventilation in pigs: the effects of desflurane, isoflurane, and propofol.

OBJECTIVE: To study how desflurane, isoflurane, and propofol affect pulmonary perfusion, shunt fraction, and systemic oxygenation during one-lung ventilation (OLV) in vivo. DESIGN: Prospective animal study with a crossover design. SETTING: Animal laboratory of a university hospital. PARTICIPANTS: Twelve female pigs. INTERVENTIONS: The pigs were anesthetized, tracheally intubated, and mechanically ventilated. After placement of femoral arterial and thermodilution pulmonary artery catheters, a left-sided, double-lumen tube (DLT) was placed via tracheotomy. After DLT placement, F(I)O(2) was adjusted at 0.8, and anesthesia was continued in random order with 1 minimal alveolar concentration of desflurane, 1 minimal alveolar concentration of isoflurane, or propofol. MEASUREMENTS AND MAIN RESULTS: Measurements of respiratory and hemodynamic parameters were made after stabilization at each anesthetic. During OLV, perfusion of the nonventilated lung and shunt fraction were comparable during all 3 anesthetics. PaO(2) was lower during desflurane and isoflurane anesthesia as compared with propofol anesthesia. Mixed venous PO(2) and cardiac output were lower with desflurane and isoflurane as compared with propofol. CONCLUSIONS: In a clinically relevant model of OLV cardiac output, PaO(2) and mixed venous PO(2) decreased during desflurane and isoflurane as compared with propofol, whereas perfusion of the nonventilated lung and shunt fraction remained comparable.

Protection with antibody to tumor necrosis factor differs with similarly lethal Escherichia coli versus Staphylococcus aureus pneumonia in rats.

BACKGROUND: Differing factors may alter the effects of antibody to tumor necrosis factor (TNF) in infection and sepsis. The authors tested whether bacteria type or treatment route alters antibody to TNF in a rat model of bacterial pneumonia. METHODS: Rats (n = 231) received similarly lethal doses of either intratracheal Escherichia coli or Staphylococcus aureus followed by treatment with either intratracheal or intraperitoneal antibody to TNF or control serum. Animals received antibiotics (cefotiam daily dose, 100 mg/kg) starting 4 h after inoculation and were studied for up to 96 h. RESULTS: Compared with S. aureus, E. coli increased serum TNF and interleukin-6 concentrations, lung lavage TNF concentrations, neutrophil counts, and alveolar-to-arterial oxygen gradients and decreased circulating neutrophils and lymphocytes (P > or = 0.05 for all). Compared with controls, with both bacteria, except for lung lavage TNF concentrations (which decreased with intratracheal but not with intraperitoneal antibody to TNF), treatment route did not alter the effects of antibody to TNF on any parameter (P = not significant for all). Antibody to TNF reduced mortality rates (relative risk of death +/- SEM) with both E. coli (-1.6 +/- 0.6; P = 0.006) and S. aureus (-0.5 +/- 0.04; P = 0.185), but these reductions were greater with E. coli than with S. aureus in a trend approaching statistical significance (P = 0.09). Compared with controls, similarly (P = not significant) with both bacteria, antibody to TNF decreased lung lavage and tissue bacteria concentrations (both P < 0.05) and serum TNF concentration (P < 0.09) and increased circulating neutrophils and lymphocytes (both P < or = 0.01). Compared with S. aureus, with E. coli antibody to TNF decreased alveolar-to-arterial oxygen gradients (P = 0.04) and increased serum interleukin-6 concentrations (P = 0.003). CONCLUSION: Antibody to TNF improved host defense and survival rates with both lethal E. coli and S. aureus pneumonia, but protection was greater with E. coli, where TNF concentrations were higher than with S. aureus. The efficacy of antiinflammatory agents in sepsis may be altered by bacteria type.