WPŁYW NIEINWAZYJNEJ WENTYLACJI MECHANICZNEJ NA ODCZUWANIE DUSZNOŚCI, STAN KLINICZNY I PROCES DIAGNOSTYCZNY W POCHP

Szymon Skoczyński1, Patrycja Rzepka-Wrona1, Antonio M. Esquinas2, Władysław Pierzchała1, Adam Barczyk1

1KLINIKA PNEUMONOLOGII, GÓRNOŚLĄSKIE CENTRUM MEDYCZNE IM. PROF. L. GIECA ŚLĄSKIEGO UNIWERSYTETU MEDYCZNEGO W KATOWICACH, KATOWICE, POLAND

2NTENSIVE CARE UNIT AND NON INVASIVE VENTILATORY UNIT, HOSPITAL GENERAL UNIVERSITARIO MORALES MESEGUER, MURCIA, SPAIN

ABSTRACT

Chronic obstructive lung disease (COPD) is a common life-threatening disease characterized by exposure to tobacco smoke, dyspnea and persistent lower airway obstruction coexistence of COPD and chronic heart failure (HF) may present a considerable challenge during both diagnostic and therapeutic processes.

Herein, we report an elderly, obese male, an ex-smoker, suffering from both COPD and HF, and treated according to the applied guidelines for 15 years. On admission to hospital, the patient was diagnosed and treated for severe type 2 respiratory failure. The patient’s COPD diagnosis was questioned at first, but then reconsidered after treatment described below. Noninvasive ventilation (NIV) improved the patient’s clinical condition and reduced his dyspnea sensation. As a consequence, during check-ups, spirometry maneuvers could have been performed properly, revealing the underlying bronchial obstruction, which had been beforehand concealed by debilitation of respiratory muscles and decreased lung tissue compliance in a patient with chronic HF.

Conclusion: NIV application in a patient with type 2

respiratory failure may significantly improve one’s clinical condition, reduce dyspnea sensation and help establish an accurate diagnosis.

STRESZCZENIE

Przewlekła obturacyjna choroba płuc (POChP) to często występująca, prowadząca do śmierci choroba, która charakteryzuje się wywiadem narażenia na dym tytoniowy, dusznością oraz obecnością utrwalonej obturacji dolnych dróg oddechowych. Współistnienie POChP i przewlekłej niewydolności serca (PNS) może powodować trudności w procesie diagnostyczno-terapeutycznym.

Niniejszym przedstawiamy przypadek starszego, otyłego mężczyzny, byłego palacza tytoniu, leczonego z powodu PNS i POChP, które były leczone farmakologicznie przez ostatnich 15 lat według ówcześnie obowiązujących wytycznych. Przyczyną pierwszej hospitalizacji była diagnostyka i leczenie ciężkiej przewlekłej całkowitej niewydolności oddychania. Podczas pierwszej hospitalizacji diagnoza POChP została zakwestionowana, jednak rozważono ją ponownie po zastosowaniu terapii opisanej poniżej. Nieinwazyjna wentylacja mechaniczna (NWM) poprawiła wydolność fizyczną pacjenta, a także zmniejszyła duszność odczuwaną przez pacjenta. W rezultacie podczas badań kontrolnych manewry oddechowe zostały wykonane prawidłowo, ujawniając obturację, utajoną uprzednio przez osłabienie mięśni oddechowych i zmniejszoną podatność płuc u chorego z PNS.

Wnioski: stosowanie NWM z całkowitą niewydolnością oddechową może znacznie poprawić stan kliniczny, zmniejszyć odczuwanie duszności i pomóc w postawieniu właściwej diagnozy.

Wiad Lek 2018, 71, 8, -1635

INTRODUCTION

A chronic obstructive pulmonary disease is a common cause of death associated with lung function deterioration, respiratory failure, and, frequent exacerbations. The disease contributes to exercise intolerance and life quality impairment. Recently, a combination of long-term oxygen therapy (LTOT) and noninvasive home ventilation have been proven to be life-prolonging in a cohort of stable COPD patients [1]. COPD diagnosis according to GOLD guidelines is established by post-bronchodilator FEV1/FVC ratio <0.7 in a symptomatic individual with the history of tobacco smoke exposure [2]. Obstructive sleep apnea syndrome (OSA) and COPD overlapping is common, being a clinical condition which also predisposes to cardiovascular comorbidities. Presence of such, along with age-related difficulties in spirometry performance exacerbate the prognosis and contribute to problems and doubts at the early stages of the diagnostic process [2].

Furthermore, cardiovascular diseases, which are a frequent cause of hospitalization and death escalate disease severity. It is vital to differentiate between COPD and COPD/HF or COPD/OSA overlap syndromes, as β-mimetics are key medications in the treatment of COPD, whereas β-antagonists are basic heart failure (HF) medications. Naturally, OSA increases the risk of heart failure, ant coincidence of COPD and HF overlap, both diseases should be treated according to their guidelines [2, 3]. However, administration of β-agonists in a dyspneic patient with pure HF might be harmful.

CASE REPORT

Herein, we report a 69-year-old male, an ex-coal miner, with a diagnosis of COPD established ten years prior. Unfortunately, a printout of previous spirometry results was unavailable. Past medical history included tobacco exposure (ca. 100 pack-years) and frequent hospitalizations due to COPD exacerbations – 4 in the last year. BODE index was 7 points. Cardiovascular comorbidities included myocardial infarction, persistent atrial fibrillation (PAF), both left and right ventricular failure, with left ventricle ejection fraction (LVEF) of 35 %, NYHA IV. Right ventricle systolic pressure (RVSP) was estimated up to 50 mmHg and throughout echocardiography revealed tricuspid annular plane systolic excursion in M-mode (TAPSE) as less than 10 mm, indicating severe RV&LV dysfunction. The patient also had type 2 diabetes and morbid obesity with body mass index (BMI) of 40.5 kg/m2. The patient was administered chronic pharmacotherapy consisting of bronchodilators (LABA, LAMA, theophylline), and other medications (diuretics, β-blocker, digoxin, ramipril, simvastatin, acenocoumarol, metphormine which was replaced by intensive insulin therapy during hospitalizations). Respiratory failure has been treated for the last six years with home oxygen therapy (HOT). On admission, the patient was in poor clinical condition, complaining of severe resting dyspnea (18/20 points in Borg scale exertion and mMRC 4 points), productive cough, excessive daytime sleepiness and nycturia. Abnormalities revealed on physical examination were as follow: central and peripheral cyanosis, peripheral edema of legs, silent and hollow heart sounds with an irregular heart rate of approximately 60/min, decreased vesicular sound with protracted expiration and bilateral fine rales at the lung base. ECG findings included atrial fibrillation, low amplitudes of QRS complexes in precordial leads, RBBB and delayed R/S transition in the precordial leads. Laboratory tests revealed polyglobulia (hemoglobin 18.3 g/dL, hematocrit 54%), no other significant abnormalities were noted. Arterial blood gas (ABG) revealed type 2 respiratory failure (Table 1).

After successful initial NIV treatment (S/T, IPAP 16 cmH2O, EPAP 8 cmH2O, I:E 1:2), the patient who was still administered bronchodilators, was subjected to clinical reassessment. The NIV treatment was well tolerated and resulted and significant clinical improvement. No side effects related to NIV were reported. Consequently, COPD diagnosis was verified, as spirometry revealed a restrictive pattern (FEV1/FVC >0.70) (MasterLab Jaeger) (Table 1). Repeatability was B in NLHEP scale, and the test was performed according to American Thoracic Society guidelines. Because of obstructive sleep apnea suspicion (7/8pts. in STOP-Bang questionnaire; 14/28 pts. in Epworth Sleepiness Scale). Type III polysomnography was performed with the use of STARDUST Respironics device, revealing moderate severity sleep apnea syndrome without significant central events; apnea-hypopnea index (AHI) of 28.7/h; obstructive apnea (OA): 12.8/h; central apnea (CA): 2.2/h. The test was performed directly after clinical stabilization and the patient was administered oxygen flow of 2L/minute. Mean and minimal oxygen saturation (SaO2) value was measured to be 89% and 56%, respectively and oxygen desaturation index (ODI) 36.7/h. The patient was assessed with six minutes walking test performed according to Polish Respiratory Society guidelines [4]. The test revealed severe exercise capacity deterioration (Tab. 1). After hospitalization due to chronic type 2 respiratory failure which was not responding to all other treatment methods, the patient was qualified for home NIV supported with oxygen due to type 2 respiratory failure and home rehabilitation program [5]. During multi-disciplinary clinical assessment it was decided that, according to current GOLD guidelines, bronchodilators should be discontinued, as it had been decided that the most probable cause for respiratory failure be obese hypoventilation syndrome (OHS). Philips Respironics Trilogy 100 respirator and an oro-nasal Philips Respironics size L mask were used. Initial settings based on the patients tolerance and ABG analysis were as follows: spontaneous over timed (S/T) mode with average volume assured pressure support (AVAPS): maximal inspiratory positive airway pressure (IPAPmax) 33 cmH2O, minimal inspiratory positive airway pressure (IPAPmin) 14 cmH2O, expiratory positive airway pressure (EPAP) 6 cmH2O, inspiration time (Ti) 1.4 s, breaths per minute (BPM) back up rate of 15/minute, target tidal volume (TV) 700 ml 7 mL/kg, rise time (RT) of 100 ms and additional oxygen supplementation of 3 L/min. NIV+ oxygen was administered for ≥8 h/day, whereas HOT alone for ≥16h/day. Baseline treatment ventilator calculated outcomes were as follows: IPAP 20 cmH2O, minute ventilation (MV) 11.9 L/min with 66% patient triggered breaths and total leak within an accepted range of 40 L/min. The rehabilitation took place twice a week at home under the supervision of professional physiotherapists. The training program consisted of walking-based endurance training, strength training, respiratory muscle training, breathing retraining techniques aimed at improvement of physical endurance and reduction of persistent dyspnea sensation [6]. Due to hypoxemia present at rest, the whole training program was performed with oxygen supplementation 3 L/min through a nasal cannula. After prior training, the patient was advised to perform Nordic-Walking at remaining days [7]. After three months of home treatment the patient was readmitted for follow-up. His condition and physical capacity were improved (Table 1). After implementation of NIV, the patient reported no signs of excessive daytime sleepiness. Surprisingly, spirometry revealed obstruction, therefore, COPD diagnosis was re-considered (Table 1). Another case conference led to the final decision, to re-start bronchodilation treatment and to adjust NIV settings according to a new pathophysiological pattern. After four months of combined treatment (NIV + oxygen + rehabilitation and bronchodilators) the patient was admitted to our Department for the third time. It was revealed that blood oxygenation, acid-base balance and exercise capacity improved again (Table 1). Outpatient treatment was planned with well-tolerated NIV settings: S/T; AVAPS: IPAPmax 30 cm H2O, IPAPmin 14 cm H2O, EPAP 7cmH2O (increased due to hypopneas which persisted when lower EPAP levels were implemented), Ti 1.3 s, BPM 14/min, targeted TV 650 ml, RT 100 ms, oxygen supplementation at rest of 2-3 L/min. These settings resulted in effective measured treatment outcomes: IPAP 19 cmH2O, EPAP 7 cmH2O, MV 11.7 L/min, 18 BPM with 58% patient triggered breaths and a total leak of 33 L/min. The rehabilitation was continued through entire observation time. Due to significant clinical improvement and a two-year wait lists no control PSG was performed. NIV statistics readings assessed the reduction in the prevalence of sleep events. The patient remained in follow-up for three consecutive years without clinical exacerbations.

DISCUSSION

Herein, we have presented a case description which is, as we believe, of clinical importance due to potentially life-threatening consequences of COPD/OSA/HF overlapping as causes for diagnostic and therapeutic difficulties. While according to GOLD guidelines persistent bronchial obstruction is necessary to diagnose COPD [2], our patient’s case may be an example of a rare exception. In retrospection, the initial diagnosis was most probably accurate. Advanced age, concomitant diseases such as HF with pulmonary congestion, spirometry maneuvers impaired by obesity and emphysema-induced diaphragm replacement, all leading to increased work of breathing, changed respiratory pattern form pure obstructive to mixed obstruction and restriction [3]. The loss of obstructive pattern could have been caused by the presence of type 2 respiratory failure leading to progressive striated muscles’ weakness, voluntary exhalation debilitation and consciousness deterioration in an elderly patient with left heart failure [2, 3]. Obstructive spirometry pattern after NIV accompanied with rehabilitation may be explained by respiratory muscles’ function improvement, decreased air trapping and increased ventilatory response to CO2 [6, 8]. Diaphragm contractility dysfunction also correlates with nocturnal hypoxemia [9], which was revealed with polysomnography and reversed by NIV treatment. The aforementioned NIV-induced mechanisms also explain the reduction of dyspnea sensation and the improvement of physical exercise tolerance.

Moreover, body mass reduction by 11 kg (BMI 36,26 kg/m2) in the course of treatment may have had a positive impact on diaphragm contractility. Body mass reduction and increased physical activity had a positive impact on muscles’ strength and significantly improved exercise capacity [6, 7]. There is also a possibility that hypercapnia induced fluid retention resulting in interstitial tissue edema which in turn increased lung resistance. This may have been responsible for the initially falsified spirometry results [10]. We need to emphasize that the aforementioned differences in spirometry results were not caused by technical bias as all assessments were performed by the same certified technician according to current ERS guidelines. The most probable hypotheses explaining NIV benefits in our patient’s case are diminished nocturnal hypoventilation, daytime PaCO2 reduction and/or NIV-related recovery of voluntary respiratory muscles [2].

Lastly, it has been suggested that NIV improves bronchial patency and decreases pulmonary hyperinflation, thus reducing the subjective dyspnea feeling and, objectively, improving physical endurance [11]. Moreover, after NIV implementation, the patient was reassessed by a cardiologist, and significant LVEF improvement was noted. According to Carvalho LA et al., NIV administration before maximum exercise test in HF patients led to an increase in improvement in exercise tolerance due to the improvement of voluntary ventilation reserves and improvement of chronotropic heart reserves [12]. According to disease-specific indications, the NIV settings could have been considered as suboptimal [13]. However, in patients with mixed ventilatory constraint, NIV settings were settled by arterial blood gas analysis, patient tolerance and assessed minute ventilation. Clinically, the most important proof for our treatment effectiveness is dyspnea reduction (from NYHA IV to NYHA II/III) and clinically significant increase in 6MWT distance (Table 1), which reflects peripheral muscle, diaphragmatic, cardiovascular and respiratory function improvement [6]. In a recent study, beneficial effects of NIV in patients with HF and LVEF of 35 ± 15% were described, showing NIV’s effectiveness in increasing exercise tolerance and a correlation between endurance time and maximum inspiratory pressure [14]. On the basis of our report, we assume that NIV accompanied with rehabilitation is a safe and effective treatment modality, which may facilitate the diagnosis and treatment of severe COPD overlapping with OSA and/or HF. It is crucial to underline that the COPD patient with a significant number of comorbidities was treated for several months with NIV and oxygen therapy without additional bronchodilator therapy. During the second phase of treatment, the patient suffered no exacerbations. Moreover, his clinical status especially considering dyspnea assessed with mMRC scale and exercise capacity with the use of 6MWT and pulsoxymetry improved even further (Tab. 1). Adding LABA&LAMA during the third hospitalization improved the clinical status even further.

Naturally, it is impossible to determine the primary cause for the clinical improvement based solely on single case observation, which is the major limitation of this study. Further studies on patients with type 2 respiratory failure and marginal FEV1/VC ratio are required to confirm and further explain our observation.

Conclusion

COPD diagnosis in an obese patient with type 2 respiratory failure may be difficult to establish. NIV application has a potential to improve patients clinical status assessed by dyspnea and exercise capacity measurement and, subsequently, the diagnostic accuracy.

Acknowledgments

We want to acknowledge dr Jacek Nasiłowski form the Medical University of Warsaw for his substantial comments which helped improve the quality of our observation.

References

1. Köhnlein T, Windisch W, Köhler D et al. Non-invasive positive pressure ventilation for the treatment of severe stable chronic obstructive pulmonary disease: a prospective, multicentre, randomised, controlled clinical trial. Lancet Respir Med. 2014;2(9):698-705.

2. Downloaded from www.goldcopd.com

3. Roversi S, Fabbri LM, Sin DD et al. Chronic obstructive lung disease and cardiac diseases: an urgent need for integrated care. Am J Respir Crit Care Med. 2016;194(11):1319-1336.

4. Przybyłowski T, Tomalak W, Siergiejko Z et al. Polish Respiratory Society guidelines for the methodology and interpretation of the 6 minute walk test (6MWT). Pneumonol Alergol Pol. 2015;83(4):283-297.

5. Schroff P, Hitchcock J, Schumann C et al. Pulmonary Rehabilitation Improves Outcomes in Chronic Obstructive Pulmonary Disease Independent of Disease Burden. Ann Am Thorac Soc. 2017;14(1):26-32.

6. Gloeckl R, Marinov B, Pitta F. Practical recommendations for exercise training in patients with COPD. Eur Respir Rev. 2013;22(128):178-86.

7. Breyer MK, Breyer-Kohansal R, Funk GC, et al. Nordic walking improves daily physical activities in COPD: a randomised controlled trial. Respir Res. 2010;11:112.

8. Nickol AH, Hart N, Hopkinson NS et al. Mechanisms of improvement of respiratory failure in patients with COPD treated with NIV. Int J Chron Obstruct Pulmon Dis. 2008;3(3):453-462.

9. Okura K, Kawagoshi A, Iwakura M, et al. Contractile capability of the diaphragm assessed by ultrasonography predicts nocturnal oxygen saturation in COPD. Respirology. 2017;22(2):301-306.

10. Iepsen UW, Jørgensen KJ, Ringbæk T, et al. A combination of resistance and endurance training increases leg muscle strength in COPD: An evidence-based recommendation based on systematic review with meta-analyses. Chron Respir Dis. 2015;12(2):132-145.

11. Struik FM, Lacasse Y, Goldstein RS et al. Nocturnal noninvasive positive pressure ventilation in stable COPD: a systematic review and individual patient data meta-analysis. Respir Med. 2014;108(2):329-337.

12. Carvalho LA, Brandão DC, Campos SL, et al. Noninvasive Ventilation Before Maximum Exercise Test Increases Exercise Tolerance in Subjects With Heart Failure: A Crossover Study. Arch Phys Med Rehabil. 2017;98(5):849-855.

13. Skoczyński S, Tażbirek M, Pierzchała W. Non-invasive ventilation in treatment of adults with chronic respiratory failure. Pneumonol Alergol Pol. 2013;81(4):380-389.

14. Moraes IG, Kimoto KM, Fernandes MB, et al. Adjunctive Use of Noninvasive Ventilation During Exercise in Patients With Decompensated Heart Failure. Am J Cardiol. 2017;119(3):423-427.

Conflict of interest:

The Authors declare no conflict of interest.

Corresponding author

Szymon Szkoczyński

Klinika Pneumonologii Górnośląskiego Centrum Medycznego

im. prof. L. Gieca Śląskiego Uniwersytetu Medycznego

ul. Ziołowa 45/47, Katowice-Ochojec

simon.mds@poczta.fm

Received: 09.11.2018

Accepted: 26.11.2018

Table 1. Patient clinical parameters and additional test results at different treatment modalities

Assessment, Visit 1

Visit 2

Visit 3

pH (arterial blood)

7.44

7.44

7.43

PO2 (arterial blood) [mmHg]

35

42

73

PCO2 (arterial blood) [mmHg]

53

44

40

HCO3-(arterial blood) [mmol/L]

36

29

26

6MWT – distance [m]

10

210

300

mMRC

4

3

2

FEV1/FVC

0.713

0.685

0.697

FEV1 [% predicted]/[L]

44.4/1.10

56.6/1.39

55.8/1.36

FVC [% predicted]/[L]

48.5/1.50

64.2/2.03

62.1/1.95

Transcutaneous SpO2 during NIV [%]

80-85

85-93

90-93

SpO2 on oxygen [%]

60-80

80-85

80-86

SpO2 without oxygen or ventilation [%]

50-60

60-80

60-80

Table legend:

Visit I – Standard COPD pharmacotherapy + home oxygen therapy + rehabilitation

Visit II – NIV+ home oxygen therapy + rehabilitation

Visit III – NIV+ home oxygen therapy + rehabilitation + standard COPD pharmacotherapy

FEV1 -– post salbutamol forced expiratory volume in 1 second;

FVC – post salbutamol forced vital capacity;

6MWT – six-minute walking test