Anesthesia in COPD patients - Draeger

© Drägerwerk AG & Co. KGaA 1

With the number of COPD patients rising worldwide, it is imperative that the optimal ap-proach of anesthesia in these patients is well known: Even stable COPD patients have an up to fourfold increased risk of postoperative pulmonary complications, which may result in a significant clinical impact of increased mortality and morbidity.1 The following text offers a brief and concise overview of recommendations from current literature as well as expert opinion for the perioperative phase.

Anesthesia in COPD patients: aspects to keep in mind

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ANESTHESIA IN COPD PATIENTS: ASPECTS TO KEEP IN MIND

– Where applicable: chest x-ray, spiroergometry, blood gas analysis, echocardiography (beware: up to 30% pulmonary hypertension [PAH] in COPD patients, associated with significantly increased morbidity and mortality).2

– Elective surgery only for infection-free patients on optimal COPD therapy. • Moderate COPD has a higher incidence of postoperative pulmonary infection than mild disease > early treatment reduces the

incidence of postoperative pulmonary infection.3 • If early treatment / optimization of treatment is not possible, even an adaptation a few days before surgery could be beneficial.*– Screen (and treat) patients for malnutrition: albumin < 3.5mg/dl is a strong predictor of postoperative pulmonary complications

(PPC).4

– Premedication without benzodiazepines, as these may blunt response to hypoxia and hypercarbia in addition to reduction in respiratory drive.5

– Determine physical fitness and ASA status (ASA III patients have 3x higher PPC risk, ASA IV 5x than ASA I).6

OTHER RISK FACTORS FOR PPC:– Strong predictors of PPC are a positive cough test (involuntary cough after deep inspiration) and smoking more than

40 pack years.7 – Wheeze, prolonged expiration.5 – Decreased pulmonary function and longer intraoperative ventilation.3

– ARISCAT score to estimate PPC risk: age, low preoperative room-air SpO2, respiratory infection in the month prior to surgery, preoperative anemia (≤ 10g/dl), surgical site of incision (intrathoracic incision has a higher risk than abdominal site), duration of surgery and emergency procedure.8

1. PRE-OPERATIVE PHASE

PATIENT PRE-HABILITATION Aim of prehab: reduce side effects of medical/surgical interventions:– If possible, patients should undergo physiotherapeutic

exercises (to reduce the incidence of intraoperative bronchial plugging or pneumonitis) and endurance training (for pulmonary rehabilitation).9

– Weight loss: BMI ≥30kg/m2 associated with PPC.10

– Smoking stop: The largest effect has been shown when smoking stop starts 4-8 weeks preop, but other investigations have failed to confirm these findings.5

– Most centers therefore advocate stopping smoking regardless of the interval before surgery.5

Useful link: ARISCAT score calculator my MDCALC

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https://www.mdcalc.com/ariscat-score-postoperative-pulmonary-complications



GENERAL NOTES– Keep anesthesia time to a minimum: Procedures > 3h significantly increase PPC risk.7

• Keep actual surgery as short as possible. • Ensure good overall management of surgery (avoid long waits for surgeon etc.).– Use pre-warming and intraoperative warmth management: moderate levels of hypothermia (34-35°C) have been associated with

higher incidences of myocardial ischemia and surgical site infection.7

– A volume-restrictive approach decreases the risk of pulmonary edema.5

– If necessary (but especially in GA), pre-oxygenation with elevated upper body and CPAP. • Pre-oxygenation for any patient hypoxic on air before induction.* • In patients with severe COPD and hypoxia, CPAP during induction may be used to improve the efficacy of pre-oxygenation and

reduce the development of atelectasis.5

– Any bronchospasm should be treated promptly (inhaled bronchodilators or deepening anesthesia with propofol or increased concentrations of volatile anesthetics).5

– Volatile anesthetics (isoflurane, sevoflurane, not desflurane) are preferable for maintenance of anesthesia due to their bronchodilatory effect).5

• Use normal dosage, volatile anesthetics can easily be adapted during surgery.*

CHOICE OF ANESTHETIC– Preference for regional anesthesia (RA) (spinal anesthesia, peripheral nerve block, combined spinal / epidural anesthesia) rather

than general anesthesia (GA).* – Benefits of RA: • Reduction of PPC of up to 50%.11

• Lower incidence of postop pneumonia, reduced ventilator dependence and unplanned postoperative intubation.12

• Superior postoperative analgesia without risking respiratory depression.13

– Attention regional anaesthesia: reported unintentional phrenic nerve palsy rates between 100% (older studies and landmark-guided approach) and 33% (newer studies with ultrasound-guided procedures), which may result in diaphragm paresis and sympathetic blockade (bronchoconstriction), potentially causing respiratory complication and necessitating intubation / re-intubation.5

– Generous indication for epidural anesthesia within perioperative pain therapy of both RA and GA: recent evidence shows reduction of PPC.14

IF GENERAL ANAESTHESIA IS USED:– Comprehensive pre-operative evaluation.15

– Place arterial catheter for BP monitoring and blood gas analysis.9 – Avoid tracheal intubation (associated with increased morbidity due to stronger manipulation of the airways),

use laryngeal mask airway or similar where possible.5

2. INTRAOPERATIVE PHASE



Increased incidence of adverse respiratory events may be expected for: – age > 60f.– spirometric changes (FEV1< 1l).– upper torso surgeries.– preoperative use of nasogastric tube.5

NEUROMUSCULAR RELAXATION– Long acting muscle relaxants (pancuronium) and opioids (morphine) are associated with increased PPC risk.5

– Use short-acting relaxants or avoid relaxants if possible.5

– Residual neuromuscular blockade is a major predictor of PPC.5

– Generous indication for the use of relaxometry to reduce risk for residual blockade.5

– Aim for TOF ratio of 0.95 to reduce the risk of silent regurgitations.5

– Antagonization: sugammadex vs neostigmine • Neostigmine has unfavorable side effect profile in COPD patients.* • Sugammadex associated with decreased respiratory failure, pleural effusion, and atelectasis.22

• The benefits of sugammadex are consistently observed in various high-risk subgroups of old age, bronchiectasis, and prolonged general anesthesia as well as in patients with various airflow limitation degrees (mild to very severe).22

MECHANICAL VENTILATIONLung-protective ventilation to reduce PPC risk.16

– Tidal volume • The LAS VEGAS trial concluded that a large portion of patients receive high tidal volumes.26 Also, from daily practice it seems

that anesthesiologists frequently employ volumes of > 10ml/kg/BW, believing that lower tidal volumes are harmful. However, lower tidal volumes of 6ml/kg predicted BW are not harmful and do not increase the risk of atelectasis.17 In fact, lower tidal volumes are explicitly recommended.

• Higher tidal volumes (12 vs. 6 cm H2O) were associated with poorer postoperative lung compliance, higher risk of barotrauma and increased intrapulmonary shunt.17

– PEEP • Moderate PEEP may facilitate expiration and reduce inspirational breathing effort.18 • 5-8 as a general rule.* • Patients on PEEP 5 have significantly better oxygenation, better pulmonary compliance, less postoperative atelectasis and

significantly fewer PPC.17

• Higher PEEP is not necessary for most patients, but can be considered for patients at very high risk for atelectasis or with concomitant lung injury.17

• The use of low tidal volume and zero or low PEEP leads to increased lung inflammation and 30 day mortality.17



– Recruitment maneuvers (RM)8

• RM have been shown to improve oxygenation and pulmonary physiology and to reduce postoperative pulmonary complications in at risk patient groups, including COPD patients. Studies have also shown improved pulmonary function tests, fewer alterations in chest radiographs, and higher postoperative arterial oxygen saturation.16

– Mind the driving pressure* • In patients on controlled mechanical ventilation, the driving pressure of the respiratory system is defined as the difference between

plateau pressure and positive end-expiratory pressure (Pplat-PEEP), and can also be expressed as the ratio of tidal volume to respiratory system compliance (Vt/Crs).20

• When establishing PEEP level, driving pressure should decrease. Keep driving pressure at < 15cm H2O. • Limit inspiratory pressure < 30cm H2O.

– Aim for minimal FiO2: • High FiO2 (80%) doubles PPC risk.17

• A frequent approach in practice is to preoxygenate with high FiO2 followed by down-titration after intubation. Rule of thumb: SpO2 of ~93%.*

– Possible advantages PCV vs. VCV ventilation • Investigations of supposed superiority of pressure vs. volume controlled ventilation have had marginal or conflicting results.17

• Significantly lower peak inspiratory pressure.21

• There is evidence of improved oxygenation in PCV.21

– I:E ratio • Adapt I:E ratio (typically to 1:3 to 1:5): A long expiratory time allows complete exhalation, avoids air trapping and reduces

‘breath-stacking’ and intrinsic PEEP (PEEPi).5

PLEASE NOTE: – Recent data suggest that RM may not confer a benefit when used solely as an adjunct to conventional ventilation:

This strategy has been shown to lead to increase PPCs and intraoperative oxygen desaturation vs. a low tidal volume, moderate PEEP ventilation.17

– The benefit of RM may therefore be most pronounced when incorporated into a package of intraoperative lung protective ventilation (i.e. PEEP of at least 5 cm H2O PEEP, a tidal volume of 6-7 mL/kg PBW or below).17

– Use a slightly lower pressure level when performing RM in COPD patients (vs. lung-healthy patients).*– Perform RM with anesthesia device (not manually!). This will help to prevent high pressures and not lose the

subsequent PEEP level.*– It is important to maintain an adequate PEEP level after RM in order to prevent de-recruitment (this is particularly

significant for adipose COPD patients).19

– After 5-6 breaths or when saturation increases, switch back to lung protective ventilation.*– As confirmed in studies, RM should always be conducted together with other measures (lung protective ventilation,

fluid restriction, warmth management).*



– Close monitoring recommended - COPD patients remain high risk patients even after Extubation Extubation does not mean the critical phase is over, on the contrary: This is the vulnerable phase. If patient cannot take CPAP,

high-flow nasal oxygen (HFNO) is a good alternative, but only in the PACU or on the ICU with O2 wall supply! During transport, nasalhigh-flow is unsuitable due to high O2 use (up to 60l/min) and rapid depletion of oxygen cylinders.*

– In GA, peri-extubation bronchodilator treatment may be helpful.9

– Transferal from OR to recovery room is a critical phase, COPD patients lying on their backs in a flat position can easily reach state of critical deoxygenation. Make sure of appropriate positioning of patient, O2 supply, and controlled exit from the OR.*

– Logistics are frequently the stumbling block: Try to organize direct repositioning into bed and avoid long periods of lying in supine position.*

– Routine prophylactic noninvasive CPAP postoperatively for the reduction of PPC has the potential to be used in practice, despite a current lack of data.1

– In patients with regional anaesthesia and subsequent ipsilateral diaphragm palsy, use sonography to secure diagnosis. In this case it is probably expedient to keep patient on CPAP support until the local anesthetic has worn off. Reintubate if necessary.*

– Note the bimodal course of respiratory complications: The first peak is immediately after surgery, the second peak on 2nd/3rd postoperative day. In practice, this means: increased postoperative vigilance, if possible abstain from benzodiazepines / opiates in unnecessary high dosage to avoid respiratory issues, and wherever possible introduce physiotherapy and early mobilization.*

– Attention thrombosis prophylaxis: Patients with COPD stage III/IV have a two-fold higher risk of secondary VTE compared to subjects with normal airflow; COPD patients with VTE have a substantially higher mortality rate than those without (50.2% vs 5.6% per year).23

– If necessary: postoperative control on ICU or intermediate care ward.

PLEASE NOTE: ONE LUNG VENTILATION IN COPD PATIENTSIn general, the same approach as illustrated above also applies to one-lung ventilation. However, the remaining lung should be treated with extreme protection, always proceed with maximum caution. In addition, the use of intraoperative TEE is recommended in case of unexpected haemodynamic deterioration.*

3. POSTOPERATIVE PHASE

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COPD PATHOPHYSIOLOGYAirway obstruction Increased resistance of the small conducting airways and increased compliance of the lung leads to a prolonged time constant. FEV1 and (FEV1/FVC) are reliable screening tools because they are affected by both airway obstruction and emphysema. Note: Unlike asthma, reduced FEV1 in COPD seldom shows large responses to inhaled bronchodilators.

Dynamic hyperinflation and PEEPiDuring spontaneous breathing, the respiratory system may fail to reach passive functional residual capacity (FRC) at end-expiration, known as dynamic hyperinflation. The breathing pattern is often such that expiration is interrupted before the alveolar pressure has decreased to atmospheric pressure, leading to an increase of the end-expiratory lung volume above the FRC. This PEEP in the alveoli at rest has been termed “auto-PEEP” or “PEEPi”. COPD patients can have an increased inspiratory load, on top of their already increased expiratory load.

Gas exchange impairmentVentilation/ perfusion (V/Q) mismatching causes reduction in

PaO2, but shunting is minimal. Thus, slightly elevated inspired oxygen is effective in treating hypoxemia due to COPD. If hypercapnia is present, it reflects both V/Q mismatching and alveolar hypoventilation, the latter resulting from both respiratory muscle dysfunction and increased ventilatory requirements.

Respiratory muscle dysfunctionHyperinflation may flatten the diaphragm, leading to a decreased zone of apposition between the diaphragm and the abdominal wall, hindering rib cage movement and impairing inspiration; shorter muscle fibers in the diaphragm are less capable of generating normal inspiratory pressures; and the flattened diaphragm must generate greater tension to develop transpulmonary pressure required to produce tidal breathing.

Extrapulmonary effectsCOPD also has systemic effects, including weight loss, nutritional abnormalities and skeletal muscle dysfunction. Cardiovascular dysfunction is usually related to acute and chronic blood gas derangement, dynamic hyperinflation and increased right ventricular afterload, while pulmonary hypertension is increasingly seen as a contributing factor to COPD morbidity and mortality.

POSTOPERATIVE PULMONARY COMPLICATIONS (PPC)

– Any respiratory event up to 5-7 postoperative days.14

– PPC include respiratory failure, ARDS, atelectasis, pleural effusion, pneumothorax and bronchospasm.14

– Incidence estimated at 5-40%, PPC-associated mortality estimated at 18%.24

– Prevalence of PPC is higher in COPD patients than those with normal spirometry (30.1 vs. 10.0%).25

– Age, upper abdominal surgery and long surgery time are risk factors of PPC for COPD patients.26

COPD is a combination of inflammatory small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), leading to poorly reversible narrowing of the airway, remodeling of airway smooth muscle, increased numbers of goblet cells and mucus-secreting glands and pulmonary vasculature changes resulting in pulmonary hypertension. COPD may be hard to differentiate from asthma, transition to COPD may be fluent.5



1. Ball L et al, Curr Opin Crit Care 2016;22:379-385

2. Elwing J et al, In J Chron Obstruct Pulmon Dis 2008;3(1):55-70

3. Ji X et al, J Infect Public Health 2020;13(2):281-286

4. Edrich T et al, Curr Opin Anaesthesiology 2010;23:18-24

5. Duggappa DR et al, Indian J Anaesth 2015;59:574‐83

6. Mowery N, Surg Clin N Am 2017;97:381-1397

7. Licker M et al, Int J Chron Obstruct Pulmon Dis 2007;2(4):493-515

8. Gupta S et al, J Anaesthesiol Clin Pharmacol 2020;36(1):88-93

9. Lumb A et al, Cont Edu in Anaesth Crit Care & Pain 2014;14(1):1-5

10. Agostini P et al, Thorax 2010;65:815-818

11. Van Lier F et al, Anesthesiology 2011;115:315-321

12. Hausman MS et al, Anesth Analg 2015;120:1405-1412

13. Khetarpal R et al, Anesth Essay Res. 2016;10(1):7-12

14. Odor PM et al, BMJ 2020;368:m540

15. Costescu F, Slinger P, Current Anesthesiology Reports 2018;8:52-58,

https://bit.ly/358nn1S

16. Ladha K et al, BMJ 2015;351:h3646

17. O’Gara B et al, BMJ 2018;362:k3030

18. 22nd Congress of the German Society for Anesthesia and Intensive Care Medicine

(DGAI), statement Prof. Rolf Dembinski, Head of the Clinic for Intensive Care

Medicine and Emergency Medicine, Klinikum Bremen Mitte

19. Bluth T, Güldner A, Anästh Intensivmed 2020;61:126–136

20. Aoyama H et al, J intensive Care 2018, https://doi.org/10.1186/s40560-018-0334-4

21. Kim KN et al, BMC Anesthesiol 2016;16(1):72

22. Park S et al, J Clin Med 2020;9(1):150

23. Børvik T et al, European Respiratory Journal 2016 47: 473-481

24 Patel K et al, Perioper Med (Lond) 2016;5:10

25. Kim ES et al, Int J Chron Obstruc Pulmon Dis 2016;11:1317-1326

26. LAS VEGAS Investigators, Eur J Anaesthesiol 2017;34(8)

SOURCES:

IMPRINTGERMANYDrägerwerk AG & Co. KGaAMoislinger Allee 53–5523542 Lübeck

www.draeger.comDiscover more on our website www.draeger.com

* Dr. Steffen Seemann, MD

Senior physician anesthesiology and intensive care medicine

Clinic for Anesthesia and Intensive Care Medicine

GPR Clinic Russelsheim

Germany

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Anesthesia in COPD patients - Draeger