Hipoxia Durante Cirugia Toracica. Un Consejo Practico Para Todo Anestesiologo

8/13/2019 Hipoxia Durante Cirugia Toracica. Un Consejo Practico Para Todo Anestesiologo.

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Hypoxia During Thoracic Surgery:

Practical Advice for the Anesthesiologist

Javier H. Campos, MDProfessor

Director of Cardiothoracic Anesthesia

Vice Chair for Clinical AffairsExecutive Medical Director Operating Rooms

University of Iowa Health Care


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Introduction

Lung separation with the use of a double-lumen tube (DLT) or bronchial blocker (BB) is used to provide one-lung

ventilation (OLV) in patients undergoing thoracic, mediastinal, cardiac, vascular or esophageal procedures. [1-2]

During OLV, an intrapulmonary shunt, related in part to collapse of the non-dependent lung and increasedatelectatic areas in the dependent lung, results in hypoxemia. [3] Hypoxemia by definition is a decrease in arterial

oxygen saturation (SpO2) to less than 90% [4], or a PaO

230 Kg-m2) undergoing thoracic surgical procedures under OLV have been shown todevelop intraoperative hypoxemia and an increase in alveolar arterial oxygen difference. [12] In a study by

Schwarzkopf, et al [10], they found that patients undergoing lobectomy and pneumonectomy had better oxygenation

during OLV than patients undergoing video thoracoscopic metastasectomy. Lung perfusion studies in these patientsshowed that perfusion of the non-ventilated lung was more impaired in patients presenting for lobectomy and

pneumonectomy than in patients presenting for metastasectomy. Patients with previous lobectomy requiring

another surgery in the contralateral lung may be at risk of developing hypoxemia during total lung collapse.

Effects on Arterial Oxygen Tension (PaO2) in Supine or Lateral Decubitus Position in Thoracic Surgery

In general, for thoracic surgical patients undergoing OLV, the most common practice is to operate in a lateral

decubitus position. Therefore, gravity is a major determinant of shunt fraction and perfusion. [13] Recent studies

[14-15] have examined the changes in arterial oxygen tension (PaO2) during procedures requiring OLV. In theWatanabe, et al study [14], patients were ventilated with a FiO2 of 1.0 and divided into three groups. One group

was supine, another group was positioned in a left semi-lateral decubitus position and the third group was placed in

left fulllateral position. In the supine position group, 9 out of 11 patients had arterial oxyhemoglobin saturation


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Effects of Hypoxia on Inflammatory Response and Cytokine Release During One-Lung Ventilation

When considering the effects of ventilation on arterial oxygenation during OLV, it is better to consider the blood

flow through the unventilated lung (V/Q = O) separately from the ventilation of the low V/Q areas of the ventilated

lung. In general, the Qs/Qt fraction seen during anesthesia and OLV ranges from 15-40%.

During OLV, the non-dependent (operated) lung remains atelectatic and hypoperfused because of hypoxic

pulmonary vasoconstriction (HPV). Thus, the HPV in the non-dependent lung ameliorates the pulmonaryventilation/perfusion relationship, preserving the systemic oxygenation by constricting pulmonary vessels in poorly

ventilated or atelectatic hypoxic lung regions to divert the pulmonary blood flow to better aerated areas.[18]

Although HPV decreases the shunt fraction and attempts to resolve hypoxemia[19], it is a serious aggravating factor

when ventilation is restored because pulmonary re-expansion promotes the re-entry of oxygen through the airways,causing the release of excessive oxidative radicals.[20] The re-expansion of a previously collapsed lung is

accompanied by an ischemia/reperfusion like response resulting in the release of cytokines from the collapsed lung

and the contralateral lung. Through this mechanism, OLV increases the risk of developing acute lung injury (ALI).

[21]

During OLV, inflammatory response reactions can be produced by multiple factors such as mechanical damage due

to surgical manipulation, OLV induced atelectasis and re-expansion, atelectasis, and damage by high oxygen tensionor by the use of high peak inspiratory pressure during mechanical ventilation. [22-25] Inflammatory cytokines,

tumor necrosis factor, interleukin (IL) IB, IL-6 and IL-8 are important chemoattractants that affect the recruitmentof neutrophils and alveolar macrophages. Alveolar macrophages secrete biologically active products and thereby

play a significant role in regulating pulmonary inflammatory reactions. An increase in these inflammatory cytokinescan be clinically relevant to pulmonary complications and impairment of oxygenation during or following thoracic

surgery.

One study [25] has shown that the epithelial lining fluid contained significantly increased levels of interleukins inthe dependent or ventilated lung and the non-dependent lung at the end of thoracic surgery. The inflammatory

response was even greater in the dependent lung. The peak inspiratory pressures used in this study were below 30

cmH2O, tidal volume of 6 ml/Kg and FiO2of 0.6-1.0. Misthos, et al [26], has shown that patients with non-small cell

lung cancer have a higher production level of oxygen free radicals than the normal population; mechanicalventilation and surgical trauma are weak free radical generators. Manipulated lung tissue is also a source of free

radicals in the intra or postoperative period and lung re-expansion provoked severe oxidative stress. Interestingly,

this study also showed that the degree of generated oxygen free radicals was associated with the duration of OLV.

Oxygen toxicity is a well-recognized consequence of prolonged exposure to high FiO2characterized by

histopathologic changes similar to ALI. Oxygen toxicity occurs during OLV and involves ischemia-reperfusion

injury and oxidative stress. [27] Collapse of the operative lung and surgical manipulation result in relative organ

ischemia and reperfusion at the time of lung expansion, which leads to the production of radical oxygen species.Increasing the duration of OLV and the presence of tumor also increases the markers of oxidative stress. Lung re-

expansion should likely occur at a lower FiO2as hypoxemic reperfusion has been shown to attenuate reperfusion

syndrome.

Influence of Protective Ventilation, Continuous Positive Airway Pressure (CPAP), Positive End Expiratory

Pressure (PEEP) and Selective Lobar Ventilation in the Management of Hypoxia During OLV

Malposition of lung isolation devices is a common cause of hypoxemia. A study by Inoue, et al [5], has shown that

patients who experience DLT malposition after turning the patient into lateral decubitus position had more

malpositions during OLV and more hypoxemia. Also, this study showed that after correction of the malposition, the

patients required more interventions (i.e. CPAP or apneic oxygen insufflation) to treat the hypoxemia.

If during OLV the patient experiences hypoxemia, the first step is to ventilate the patients lung with FiO21.0 and

restore two lung ventilation. Once oxygenation improves, reassessment of the lung isolation device takes

precedence (expands the non-ventilated lung and re-assesses the position of the DLT or a bronchial blocker with the


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[38] Recent research has recommended the use of low tidal volumes during thoracic surgical procedures and during

OLV. One study [39] has shown that low tidal volume of 6 ml/kg during OLV with the use of FiO2= 0.6-0.7 and

CPAP 5 cmH2O to the non-dependent lung lead to a higher PaO2(14182 vs 11249) mmHg when compared to low

tidal volumes and PEEP 5 cmH2O to the dependent lung.

Also, alveolar recruitment maneuvers have been recommended to improve oxygenation during OLV. Tusman, et al

[40], have shown the beneficial effects with an alveolar recruitment maneuver with pressure controlled ventilation.

They reported that PaO2values were similar to the ones obtained during two lung ventilation.

During OLV it is not uncommon to alternate from volume controlled ventilation to pressure controlled ventilation in

order to improve oxygenation. One study has demonstrated that a better oxygenation is achieved when pressure

controlled ventilation is used during OLV. [41] However, another study [42] in a crossover experiment involving

thoracic surgical patients requiring OLV showed that arterial oxygenation was similar in the groups that received

volume controlled ventilation when compared to pressure controlled ventilation. Also, this study observed a

decrease in peak plateau pressure in the patients that received pressure controlled ventilation. The use of pressure

controlled ventilation would be more beneficial in the morbidly obese patient undergoing OLV. (Personal report this

study is underway) to demonstrate the advantage of this mode of ventilation to maintain optimal oxygenation during

OLV.

Pharmacologic interventions have been studied to control pulmonary blood flow during OLV. [43-46] Some studies

have shown that the use of a respiratory stimulant, such as almitrine intravenously and with an infusion, improved

oxygenation during OLV, probably due to the molecular mechanisms of action on the pulmonary vessels combined

with direct stimulation of chemoreceptors and direct pulmonary vasoconstrictive action. [43] Also, others have

shown no effect on oxygenation when inhaled nitric oxide has been used in patients requiring OLV. [44] However,

the combination of inhaled nitric oxide with intravenous almitrine has shown promising results while improving

PaO2during OLV. [45-46] At the present time, I believe these drugs are in the experimental phase to recommend

routine use to improve oxygenation during OLV.

Influence of Anesthetics on Hypoxia During the Intraoperative Period and Potential Complications in thePostoperative Period

In the 1980s, special attention was given to the effects of anesthetics and HPV during OLV. However, in the past10 years more attention has been given to the effects on ventilation, and the inflammatory response and their

potential complications after OLV, which is the development of ALI. Some of the studies have included very

limited samples of studied patients. One study [24] has shown that the use of small tidal volumes (5 ml/kg) during

OLV had lower levels of interleukin (IL-8, 10, and TNF) when compared to high tidal volumes of 10 ml/kg. Others

have shown a protective effect in modulating the inflammatory response when inhalational agents are used duringOLV compared to pure total intravenous anesthesia. [47-49] Reduction of inflammatory mediators had significantly

better clinical outcomes defined by postoperative adverse events such as atelectasis or systemic inflammatory

response syndrome. [48] As part of the intervention to manage hypoxemia and inflammatory response during OLV,I recommend the use of inhalational agents during the management of these patients.

Cerebral Desaturation During OLV

Another area that deserves special attention is the effect of hypoxia during OLV in relationship to a decrease in

regional cerebral oxygen saturation (SctO2) in thoracic surgical patients. There are different monitors that measure

SctO2such as the FORESIGHTor the INVOS[50, 51] monitor. These devices have been used in patients

undergoing OLV with mixed results. A study by Hemmerling et al [50] showed that an absolute value of SctO2of80% was recorded while the patients were awake; during OLV this value decreased to an average of 63%, and

during extubation it rose to 71%. Overall in the 20 patients studied, cerebral desaturation >20% was recorded from


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baseline values. Interesting in this study was the lack of correlation with SpO and PaO2. Also, no mini-mental state

examination (MMSE) test was performed to evaluate the cognitive function outcome of these patients. In another

study [51] involving 40 patients undergoing OLV, a SctO2monitor was used to measure cerebral desaturation in 28

patients; the minimum SctO2during OLV was lower than baseline value. The percentage of change was

significantly negatively correlated with preoperative respiratory function. Another study [52] showed that theduration of cerebral desaturation time during OLV correlates with the MMSE; of the 69 patients studied only 17

developed desaturation (SctO21 hour can be a potential cause for cardiovascular

complications (i.e., cardiac arrhythmias) through the generation of severe oxidative stress during re-expansion and

conversion to two-lung ventilation. However, further studies are needed to validate these results as a potential

cause/effect.

Summary

Hypoxemia during OLV is an infrequent finding, ventilatory maneuvers to optimize and improve oxygenation is

listed in table I. Inhalational agents appear to have a protective effect in controlling inflammatory response duringOLV. Low tidal volumes with PEEP in the dependent lung along with CPAP in the non-dependent lung appear to

be the most common intervention to treat hypoxemia [54].

Table 1: Treatment of Hypoxia During One-Lung Ventilation

Increase FiO21.0 Adjust ventilation according to patient needs pressurecontrol vs volume control?

Re-expand the collapsed lung If a DLT is being used in video thoracoscopicsurgery, consider selective O2insufflation to the non-

ventilated lung with fiberoptic bronchoscope

Convert to two lung ventilation If a bronchial blocker is used, consider selective lobarblockade in patients with previous contralateral

lobectomy

Confirm position with fiberoptic bronchoscope foroptimal position of lung isolation device

Intermittent O2insufflation with 2 l/min for shortintervals to the non-dependent lung

After SPO2>98%, convert to OLV and apply CPAP5 cmH2O to non-dependent lung

Recruitment ventilatory maneuvers during OLVUnless contraindicated (i.e. auto PEEP >10), use

PEEP 5 cm H2O routinely to the dependent lungClamping of pulmonary vessel duringpneumonectomy cases will reduce the shunt fraction


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227-246. Ed Slinger P. Springer Publisher.

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49.

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54. Campos JH. Hypoxia during Thoracic Surgery: Practical Advice for the Anesthesiologist. ASA RefresherCourse. August 20, 2013

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Hipoxia Durante Cirugia Toracica. Un Consejo Practico Para Todo Anestesiologo