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Volume 14 No. 10
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Accepted Papers





Case Reports

Tachypnea Seen During Positive Airway Pressure Titration Studies: A Case Series of Four Patients

Amit Gupta, MD; Timothy Roehrs, PhD; Kenneth Moss, MD; Syed Jaffery, MD; Luisa Bazan, MD; Laura Spear, RPSGT; Larry Darnell, RPSGT; Thomas Roth, PhD
Henry Ford Health System, Wayne State University, Detroit, Michigan

ABSTRACT

We report a case series of four patients where tachypnea was observed during positive airway titration studies, double the baseline breathing rate (tachypnea range 46–68 breaths/min). It happened mainly during non-rapid eye movement to rapid eye movement sleep transitions without significant changes in oxygen saturation or signs of autonomic hyperactivity such as an increased heart rate. The increased respiratory rate may be a normal physiological extreme outlier seen during phasic rapid eye movement sleep triggered by high pressure ventilation and it may also indicate underlying ventilatory instability, making patients predisposed to central sleep apnea.

Citation:

Gupta A, Roehrs T, Moss K, Jaffery S, Bazan L, Spear L, Darnell L, Roth T. Tachypnea seen during positive airway pressure titration studies: a case series of four patients. J Clin Sleep Med. 2018;14(10):1801–1804.


INTRODUCTION

Respiratory rate fluctuation during REM sleep has been described in humans, but these fluctuations are not more than 10%.1 In our case series, four patients undergoing positive airway pressure (PAP) titration studies had significant increase in respiratory rate, double the baseline breathing rate (baseline breathing rate range 12–26 breaths/min, tachypnea range 46–68 breaths/min) (Figure 1).

Tachypnea episodes of individual patients, as seen during positive airway pressure titration studies.

Standard polysomnography, 90-second epochs of all 4 patients.

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Figure 1

Tachypnea episodes of individual patients, as seen during positive airway pressure titration studies.

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REPORT OF CASE

Four patients underwent PAP titration studies, during the studies standard polysomnography recording (10–20 system) was used with respiratory monitoring using nasal/airflow sensors and chest/abdomen belt sensors. Sleep stage was scored utilizing American Academy of Sleep Medicine scoring criteria.2 Breathing rate was calculated by counting inspiratory flow signal peaks per minute. The tachypneic episodes were confirmed by a polysomnographic technologist and concurrent video monitoring confirmed that the episodes occurred without apparent discomfort to the patients. Apnea-hypopnea Index was calculated using current American Academy of Sleep Medicine scoring standards.2

Chart review revealed no medications that could explain the degree of tachypnea observed during the titration studies. Regarding demographics, age range for patients was 55–75 years and the body mass index range was 24–35.9 kg/m2. All patients were male. Baseline diagnostic polysomnography apnea-hypopnea index (AHI) varied from 34.4–117.4 events/h. Three of the four patients had a central apnea-hypopnea index (CAHI) > 5 events/h, which accounted for < 50% of total AHI, and the remaining patient had no central events. PAP pressure ranged from 18–25 cmH2O inspiratory positive airway pressure (IPAP) and 14–17 cmH2O expiratory positive airway pressure (EPAP). All the tachypneic events occurred mainly during rapid eye movement (REM) sleep (except one which happened only in non-rapid eye movement [NREM] sleep). Tachypneic events began during the NREM to REM transition; the events lasted between 5–20 minutes. There was no significant changes in oxygen saturation and heart rate before and during the tachypneic episodes (0% to 3% oxygen saturation variation, 3–8 bpm, respectively). Concurrent video recording demonstrated rapid shallow breathing; however, there was no significant change in flow amplitude which may be due to polysomnography software mediated digital amplitude auto correction. None of the patients had significant cardiopulmonary disease documented in their medical charts and their serum bicarbonate range was between 25–27 mmol/L.

DISCUSSION

The aforementioned tachypnea happened mainly during REM sleep and during PAP titration studies. Since there was no patient discomfort or autonomic hyperactivity such as an increased heart rate, these events were initially thought to be artifacts either due to a digital sampling errors or PAP machine related respiratory auto-triggering.

Aliasing is the misinterpretation of a signal as being a slower frequency waveform and has been well documented in literature.3 In the present cases sampling rate was low, and to further rule out sampling error we tried doing the reverse by testing normal breathing at the highest possible sampling rate. That test did not show significant change in respiratory rate as was seen during these tachypnea episodes.

As auto-triggering was also considered, we contacted the PAP machine manufacturer (Respironics) and their response was that it is not possible for their machine to trigger respiration at such a high rate. For all the four patients Respironics Omnilab Advanced PAP machine was used. Auto-triggering is associated with high mask leak.4 In our case series mask leaks during the tachypneic events ranged from 0–8 L/min except one patient who had mask leak around 40 L/min. The breathing pattern during tachypneic events was regular with no fluctuation in flow amplitude, raising low suspicion for auto-triggering. An illustration of auto-triggering can be found in Carteaux et al.4 In spite of manufacturer statement, potential machine malfunction cannot be excluded and it still remains a possibility for the observed tachypneic phenomena.

A remaining consideration is a physiological explanation for aforementioned phenomena. After a literature search we found one published case report describing REM sleep-related tachypnea to the degree seen in our studies, double the baseline breathing rate.5 However, the previous case report was observed in normal healthy volunteers and tachypnea was thought to be mediated due to direct spinal reflex pathways, to the best of our knowledge this direct spinal reflex pathway in humans has not been described anywhere else in literature yet. In our case series, chart review and data corroboration showed that events occurred during PAP titration studies with high PAP pressures (pressure ranges IPAP 18–25 cmH2O and EPAP 14–17 cmH2O). It is emphasized that the high level ventilation seen in our case series could have activated stretch receptors inhibiting breathing, yet, paradoxically, tachypnea was observed. Another finding worth noting is that all the events predominantly happened during left lateral position (Table 1), trepopnea in heart failure patients has been well described in literature, mainly in left lateral position.6,7 Possible explanations include decreased cardiac output secondary to high pulmonary capillary wedge pressure or more awareness of apical impulse in left lateral position, whatever be the reason this is often seen with sympathetic over activity. In our case series significant tachycardia was not seen before and during the events (Table 1), making this explanation less likely cause for this phenomena. Breathing control during sleep is primarily dependent on chemical/metabolic control, this is true specifically in NREM and REM tonic sleep, making respiration more regular as compared to phasic REM sleep. In phasic REM sleep, the breathing pattern is mainly affected by the behavioral system through the REM sleep processes, fluctuating with ponto-geniculo-occipital driven excitatory and inhibitory influences, making respiratory control less predictable and leading to tachypneic episodes. These fluctuations nevertheless are not more than 10%.1,8 For our four patients all the events predominantly happened in phasic REM sleep (as shown in Table 1), this finding may lead to a possible explanation as described below.

Polysomnography findings of all patients.

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Table 1

Polysomnography findings of all patients.

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We conclude that the increased respiratory rate in this series may be an extreme physiological outlier of tachypnea seen during phasic REM sleep. These tachypnea patterns were mainly seen or more robust during initial phasic REM sleep, making us wonder if this phenomena is an initial startle response to high pressure ventilation that may also be affecting cardiac output and cerebral blood flow. These tachypnea patterns may also be indicative of ventilatory instability, making patients predisposed to central sleep apnea (three out of four patients had CAHI > 5 events/h and three out of four patients were eventually started on bilevel positive airway pressure in spontaneous timed mode, during the titration studies). Although the reasons are unclear for this unique phenomena, more research is required regarding frequency of tachypnea patterns and their implications.

DISCLOSURE STATEMENT

Work for this study was performed at Henry Ford Health System/Wayne State University, Detroit, MI. All authors are in agreement with the content of the manuscript. The authors report no conflicts of interest.

ABBREVIATIONS

AHI

apnea-hypopnea index

CAHI

central apnea-hypopnea index

BPAP

bilevel positive airway pressure

CPAP

continuous positive airway pressure

CSA

central sleep apnea

EPAP

expiratory positive airway pressure

IPAP

inspiratory positive airway pressure

NREM

non-rapid eye movement

REM

rapid eye movement

PAP

positive airway pressure

PSG

polysomnography

REFERENCES

1 

Krieger J. Breathing during sleep in normal subjects. Clin Chest Med. 1985;6(4):577–594. [PubMed]

2 

Berry RB, Albertario CL, Harding SM, et al; for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Version 2.5. Darien, IL: American Academy of Sleep Medicine; 2018.

3 

Patil SP. What every clinician should know about polysomnography. Respir Care. 2010;55(9):1179–1195. [PubMed]

4 

Carteaux G, Lyazidi A, Cordoba-Izquierdo A, et al. Patient-ventilator asynchrony during noninvasive ventilation: a bench and clinical study. Chest. 2012;142(2):367–376. [PubMed]

5 

Sato S, Kanbayashi T, Kondo H, Matsubuchi N, Ono K, Shimizu T. Rapid increase to double breathing rate appears during REM sleep in synchrony with REM - a higher CNS control of breathing? Adv Exp Med Biol. 2010;669:249–252. [PubMed]

6 

Leung RS, Bowman ME, Parker JD, Newton GE, Bradley TD. Avoidance of the left lateral decubitus position during sleep in patients with heart failure: relationship to cardiac size and function. J Am Coll Cardiol. 2003;41(2):227–230. [PubMed]

7 

Fujita M, Miyamoto S, Sekiguchi H, Eiho S, Sasayama S. Effects of posture on sympathetic nervous modulation in patients with chronic heart failure. Lancet. 2000;356(9244):1822–1823. [PubMed]

8 

Xie A. Effect of sleep on breathing - why recurrent apneas are only seen during sleep. J Thorac Dis. 2012;4(2):194–197. [PubMed Central][PubMed]