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Instantaneous restoration of cardiac output by noninvasive positive pressure ventilation in a patient with obesity hypoventilation syndrome
Journal of Cardiology Cases (2011) 3, e40—e42
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Instantaneous restoration of cardiac output by noninvasive positive pressure ventilation in a patient with obesity hypoventilation syndrome Masayoshi Yoshida (MD), Shin-ichi Ando (MD, PhD) ∗, Toshiaki Kadokami (MD, PhD), Sumito Narita (MD), Hidetoshi Momii (MD, PhD), Yumi Sato (MT), Tomoko Kiyokawa (MT), Chikako Nakao (MT) Saiseikai Futsukaichi Hospital, Fukuoka, Japan Received 15 September 2010; accepted 18 October 2010
KEYWORDS Obesity hypoventilation syndrome; Sleep apnea syndrome; Heart failure; Cardiac output
Summary We report a 30-year-old man with severe obesity hypoventilation syndrome (OHVS) complicated by right-sided heart failure. Polysomnography revealed severe obstructive sleep apnea with apnea—hypopnea index (AHI) 70.4/h and gradual decrease in minimum oxygen saturation (SpO2 ) from 86% before sleep to 36% during sleep. Cardiac output (CO) was suppressed from 3.9 L/min before sleep to 2.5 L/min during sleep. Noninvasive positive pressure ventilation (NPPV) treatment drastically restored CO to the level before sleep, and improved AHI to 9.4/h and minimum SpO2 to 87%. NPPV may provide rapid and powerful symptom relief in patients with OHVS complicated with right sided heart failure. © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Introduction Obesity hypoventilation syndrome (OHVS) is defined as chronic alveolar hypoventilation in highly obese persons, and is considered to be a combination of severe obstructive sleep apnea and restrictive thoracic dysfunction [1].
∗ Corresponding author at: Department of Cardiovascular Medicine, Saiseikai Futsukaichi Hospital, Fukuoka 818-8516, Japan. Tel.: +81 92 923 1551; fax: +81 92 924 5210. E-mail address: [email protected] (S.-i. Ando).
Hypoventilation may induce pulmonary hypertension [2] and result in right-sided heart failure with symptoms such as systemic edema [3,4]. Decrease in cardiac output (CO) during single apneic period was documented in subjects with obstructive sleep apnea syndrome [5] and the B-type natriuretic peptide value was higher in sleep-disordered breathing patients [6]. However, there is no report on the time course of CO changes during the treatment period in OHVS patients. In this report, we present a case of OHVS with right-sided heart failure showing drastic improvement in CO by overnight treatment with continuous positive airway pressure (CPAP) and adaptive servo ventilator (ASV).
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jccase.2010.10.001
Noninvasive positive pressure ventilation for obesity hypoventilation syndrome
e41
Figure 1 Split-night study with polysomnography and impedance cardiometry. Initiation of continuous positive airway pressure instantaneously restored oxygen saturation as well as cardiac output and use of adaptive servo ventilator further improved the parameters to pre-sleep values. HR, heart rate; SpO2 , oxygen saturation; WK, wake; MVT, movement arousal; REM, rapid eye movement sleep; S1—4, non-rapid eye movement sleep stages 1—4; IPAP, inspiratory positive airway pressure; CPAP, continuous positive airway pressure; ASV, adaptive servo-ventilator.
Case report A 30-year-old severely obese man was transferred to our hospital for management of OHVS. He was admitted to the former hospital due to depressed consciousness with cyanosis and peripheral edema. He had been hypersomnolent for two weeks prior to admission. He was 167 cm in height and weighed 120 kg. Glasgow coma scale score was E3V5M6 without focal motor or sensory deficit. Systolic blood pressure was 90 mmHg; pulse rate was 130 bpm; and oxygen saturation (SpO2 ) on room air was 70%. Mild stridor but no cardiac murmur was noted. The initial arterial blood gas analysis on 3 L/min of oxygen through a facial mask demonstrated acidemia and hypercapnia (pH 7.218, pCO2 82.6 mmHg, pO2 99.4 mmHg, and HCO3 32.4 mmol/L). OHVS with CO2 narcosis was diagnosed and the patient was transferred to our hospital. We performed standard full polysomnography with continuous CO measurement using impedance cardiometry (PhysioFlow, Manatec Biomédical, Macheren, France) that has been validated by comparing with the Fick method [7,8]. During the first 2 h of sleep without noninvasive positive pressure ventilation (NPPV), severe obstructive sleep apnea was observed with apnea—hypopnea index (AHI) at 70.4/h (central apnea index, 0/h) and minimum SpO2 gradually decreasing to 36%, accompanied by concomitant decrease in CO to 2.5 L/min from 3.9 L/min before sleep (Fig. 1, Table 1). CPAP treatment improved AHI from 70.4 to 15.4/h and drastically increased minimal SpO2 from 36% to 82% (average
SpO2 rose from 81% to 93%), while CO increased instantaneously from 2.5 L/min to 3.7 L/min. However, because of the residual hypopnea with CPAP, we used an ASV (BiPAP Auto SV, Respironics: expiratory, minimum inspiratory and maximum inspiratory positive airway pressure were 8, 10, and 15 cmH2 O, respectively). The ASV further improved AHI to 9.4/h and minimum SpO2 to 87% (average SpO2 96%) as well as increased CO to 4.2 L/min, showing full recovery to the levels before sleep.
Table 1 Results of polysomnography and impedance cardiometry before and during sleep with and without noninvasive positive pressure ventilation. Before sleep Without NPPV
Mean SpO2 (%) 93 Minimum SpO2 (%) 86 AHI (/h) — Arousal index — CO (L/min) 3.9
81 36 70.4 57.5 2.5
During sleep With NPPV CPAP
ASV
93 82 15.4 18.5 3.7
96 87 9.4 15.8 4.2
NPPV, noninvasive positive pressure ventilation; CPAP, continuous positive airway pressure; ASV, adaptive servo-ventilator; SpO2 , oxygen saturation; AHI, apnea—hypopnea index; CO, cardiac output.
e42
Discussion We present the effect of NPPV on the change of CO in an OHVS patient complicated with right-sided heart failure. In our patient, CO as well as SpO2 decreased slowly but profoundly after falling asleep. OHVS is considered to be a combination of severe obstructive sleep apnea and restrictive thoracic dysfunction due to severe obesity. We observed gradual and continuous decreases in SpO2 and cardiac output during sleep, which are different from the brief and repetitive decreases in SpO2 and cardiac output seen in patients with uncomplicated obstructive sleep apnea syndrome [5,9]. This might be caused by pulmonary vasoconstriction resulting from hypoxia [2]. NPPV treatment increased CO and improved SpO2 presumably by instantaneously decreasing pulmonary arterial resistance. The better effect of ASV compared with CPAP may be explained by its pressure support function against respiratory restriction due to the heavy abdomen in highly obese patients. It is important to recognize that the hemodynamic status of patients with OHVS and heart conditions can be improved quickly by NPPV, especially using ASV.
Acknowledgments The patient has given informed consent for publication of the clinical data. Anonymity of the patient has been protected.
References [1] Koenig SM. Pulmonary complications of obesity. Am J Med Sci 2001;321:249—79.
M. Yoshida et al. [2] Weir EK, Archer SL. The mechanism of acute hypoxic pulmonary vasoconstriction: the tale of two channels. Faseb J 1995;9:183—9. [3] Somers VK, White DP, Amin R, Abraham WT, Costa F, Culebras A, et al. Sleep apnea and cardiovascular disease: an American Heart Association/American College Of Cardiology Foundation Scientific Statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council On Cardiovascular Nursing in Collaboration with the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health). Circulation 2008;118:1080—111. [4] Marin JM, Carrizo SJ, Vicente E, Agusti AGN. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046—53. [5] Stoohs R, Guilleminault C. Cardiovascular changes associated with obstructive sleep apnea syndrome. J Appl Physiol 1992;72:583—9. [6] Takama N, Kurabayashi M. Effectiveness of a portable device and the need for treatment of mild-to-moderate obstructive sleepdisordered breathing in patients with cardiovascular disease. J Cardiol 2010;56:73—8. [7] Charloux A, Lonsdorfer-Wolf E, Richard R, Lampert E, OswaldMammosser M, Mettauer B, et al. A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the ‘‘direct’’ Fick method. Eur J Appl Physiol 2000;82:313—20. [8] Bougault V, Lonsdorfer-Wolf E, Charloux A, Richard R, Geny B, Oswald-Mammosser M. Does thoracic bioimpedance accurately determine cardiac output in COPD patients during maximal or intermittent exercise? Chest 2005;127:1122—31. [9] Bradley TD, Hall MJ, Ando S, Floras JS. Hemodynamic effects of simulated obstructive apneas in humans with and without heart failure. Chest 2001;119:1827—35.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Instantaneous restoration of cardiac output by noninvasive positive pressure ventilation in a patient with obesity hypoventilation syndrome Masayoshi Yoshida (MD), Shin-ichi Ando (MD, PhD) ∗, Toshiaki Kadokami (MD, PhD), Sumito Narita (MD), Hidetoshi Momii (MD, PhD), Yumi Sato (MT), Tomoko Kiyokawa (MT), Chikako Nakao (MT) Saiseikai Futsukaichi Hospital, Fukuoka, Japan Received 15 September 2010; accepted 18 October 2010
KEYWORDS Obesity hypoventilation syndrome; Sleep apnea syndrome; Heart failure; Cardiac output
Summary We report a 30-year-old man with severe obesity hypoventilation syndrome (OHVS) complicated by right-sided heart failure. Polysomnography revealed severe obstructive sleep apnea with apnea—hypopnea index (AHI) 70.4/h and gradual decrease in minimum oxygen saturation (SpO2 ) from 86% before sleep to 36% during sleep. Cardiac output (CO) was suppressed from 3.9 L/min before sleep to 2.5 L/min during sleep. Noninvasive positive pressure ventilation (NPPV) treatment drastically restored CO to the level before sleep, and improved AHI to 9.4/h and minimum SpO2 to 87%. NPPV may provide rapid and powerful symptom relief in patients with OHVS complicated with right sided heart failure. © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Introduction Obesity hypoventilation syndrome (OHVS) is defined as chronic alveolar hypoventilation in highly obese persons, and is considered to be a combination of severe obstructive sleep apnea and restrictive thoracic dysfunction [1].
∗ Corresponding author at: Department of Cardiovascular Medicine, Saiseikai Futsukaichi Hospital, Fukuoka 818-8516, Japan. Tel.: +81 92 923 1551; fax: +81 92 924 5210. E-mail address: [email protected] (S.-i. Ando).
Hypoventilation may induce pulmonary hypertension [2] and result in right-sided heart failure with symptoms such as systemic edema [3,4]. Decrease in cardiac output (CO) during single apneic period was documented in subjects with obstructive sleep apnea syndrome [5] and the B-type natriuretic peptide value was higher in sleep-disordered breathing patients [6]. However, there is no report on the time course of CO changes during the treatment period in OHVS patients. In this report, we present a case of OHVS with right-sided heart failure showing drastic improvement in CO by overnight treatment with continuous positive airway pressure (CPAP) and adaptive servo ventilator (ASV).
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jccase.2010.10.001
Noninvasive positive pressure ventilation for obesity hypoventilation syndrome
e41
Figure 1 Split-night study with polysomnography and impedance cardiometry. Initiation of continuous positive airway pressure instantaneously restored oxygen saturation as well as cardiac output and use of adaptive servo ventilator further improved the parameters to pre-sleep values. HR, heart rate; SpO2 , oxygen saturation; WK, wake; MVT, movement arousal; REM, rapid eye movement sleep; S1—4, non-rapid eye movement sleep stages 1—4; IPAP, inspiratory positive airway pressure; CPAP, continuous positive airway pressure; ASV, adaptive servo-ventilator.
Case report A 30-year-old severely obese man was transferred to our hospital for management of OHVS. He was admitted to the former hospital due to depressed consciousness with cyanosis and peripheral edema. He had been hypersomnolent for two weeks prior to admission. He was 167 cm in height and weighed 120 kg. Glasgow coma scale score was E3V5M6 without focal motor or sensory deficit. Systolic blood pressure was 90 mmHg; pulse rate was 130 bpm; and oxygen saturation (SpO2 ) on room air was 70%. Mild stridor but no cardiac murmur was noted. The initial arterial blood gas analysis on 3 L/min of oxygen through a facial mask demonstrated acidemia and hypercapnia (pH 7.218, pCO2 82.6 mmHg, pO2 99.4 mmHg, and HCO3 32.4 mmol/L). OHVS with CO2 narcosis was diagnosed and the patient was transferred to our hospital. We performed standard full polysomnography with continuous CO measurement using impedance cardiometry (PhysioFlow, Manatec Biomédical, Macheren, France) that has been validated by comparing with the Fick method [7,8]. During the first 2 h of sleep without noninvasive positive pressure ventilation (NPPV), severe obstructive sleep apnea was observed with apnea—hypopnea index (AHI) at 70.4/h (central apnea index, 0/h) and minimum SpO2 gradually decreasing to 36%, accompanied by concomitant decrease in CO to 2.5 L/min from 3.9 L/min before sleep (Fig. 1, Table 1). CPAP treatment improved AHI from 70.4 to 15.4/h and drastically increased minimal SpO2 from 36% to 82% (average
SpO2 rose from 81% to 93%), while CO increased instantaneously from 2.5 L/min to 3.7 L/min. However, because of the residual hypopnea with CPAP, we used an ASV (BiPAP Auto SV, Respironics: expiratory, minimum inspiratory and maximum inspiratory positive airway pressure were 8, 10, and 15 cmH2 O, respectively). The ASV further improved AHI to 9.4/h and minimum SpO2 to 87% (average SpO2 96%) as well as increased CO to 4.2 L/min, showing full recovery to the levels before sleep.
Table 1 Results of polysomnography and impedance cardiometry before and during sleep with and without noninvasive positive pressure ventilation. Before sleep Without NPPV
Mean SpO2 (%) 93 Minimum SpO2 (%) 86 AHI (/h) — Arousal index — CO (L/min) 3.9
81 36 70.4 57.5 2.5
During sleep With NPPV CPAP
ASV
93 82 15.4 18.5 3.7
96 87 9.4 15.8 4.2
NPPV, noninvasive positive pressure ventilation; CPAP, continuous positive airway pressure; ASV, adaptive servo-ventilator; SpO2 , oxygen saturation; AHI, apnea—hypopnea index; CO, cardiac output.
e42
Discussion We present the effect of NPPV on the change of CO in an OHVS patient complicated with right-sided heart failure. In our patient, CO as well as SpO2 decreased slowly but profoundly after falling asleep. OHVS is considered to be a combination of severe obstructive sleep apnea and restrictive thoracic dysfunction due to severe obesity. We observed gradual and continuous decreases in SpO2 and cardiac output during sleep, which are different from the brief and repetitive decreases in SpO2 and cardiac output seen in patients with uncomplicated obstructive sleep apnea syndrome [5,9]. This might be caused by pulmonary vasoconstriction resulting from hypoxia [2]. NPPV treatment increased CO and improved SpO2 presumably by instantaneously decreasing pulmonary arterial resistance. The better effect of ASV compared with CPAP may be explained by its pressure support function against respiratory restriction due to the heavy abdomen in highly obese patients. It is important to recognize that the hemodynamic status of patients with OHVS and heart conditions can be improved quickly by NPPV, especially using ASV.
Acknowledgments The patient has given informed consent for publication of the clinical data. Anonymity of the patient has been protected.
References [1] Koenig SM. Pulmonary complications of obesity. Am J Med Sci 2001;321:249—79.
M. Yoshida et al. [2] Weir EK, Archer SL. The mechanism of acute hypoxic pulmonary vasoconstriction: the tale of two channels. Faseb J 1995;9:183—9. [3] Somers VK, White DP, Amin R, Abraham WT, Costa F, Culebras A, et al. Sleep apnea and cardiovascular disease: an American Heart Association/American College Of Cardiology Foundation Scientific Statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council On Cardiovascular Nursing in Collaboration with the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health). Circulation 2008;118:1080—111. [4] Marin JM, Carrizo SJ, Vicente E, Agusti AGN. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046—53. [5] Stoohs R, Guilleminault C. Cardiovascular changes associated with obstructive sleep apnea syndrome. J Appl Physiol 1992;72:583—9. [6] Takama N, Kurabayashi M. Effectiveness of a portable device and the need for treatment of mild-to-moderate obstructive sleepdisordered breathing in patients with cardiovascular disease. J Cardiol 2010;56:73—8. [7] Charloux A, Lonsdorfer-Wolf E, Richard R, Lampert E, OswaldMammosser M, Mettauer B, et al. A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the ‘‘direct’’ Fick method. Eur J Appl Physiol 2000;82:313—20. [8] Bougault V, Lonsdorfer-Wolf E, Charloux A, Richard R, Geny B, Oswald-Mammosser M. Does thoracic bioimpedance accurately determine cardiac output in COPD patients during maximal or intermittent exercise? Chest 2005;127:1122—31. [9] Bradley TD, Hall MJ, Ando S, Floras JS. Hemodynamic effects of simulated obstructive apneas in humans with and without heart failure. Chest 2001;119:1827—35.