Biographical Sketch


Hartmut Schneider,  M.D., Ph.D


Associate Professor (retired)

Johns Hopkins University, Baltimore

EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.)

Philipps-University, Marburg, Germany

Philipps-University, Marburg, Germany

Johns Hopkins University, Baltimore

M.D, Ph.D.


Assoc Prof.





Internal Medicine


  1. Personal Statement

I have more than 28 years’ experience in internal medicine and applied medical science. The recognized value of my scientific contribution to society is best illustrated by the awarded, RO1 (HL105546) and 2 recently K23 and CF foundation grants of my research fellows as well as the multiple manuscripts, some of which are detailed below.  As an accomplished scientist and clinician, it is my mission to determine the effect of sleep disorders on the progression of chronic disease.

I retired from Johns Hopkins in 2018 to better develop personalized medicine.  I therefore was privileged to be a co-founder of two Start-up companies, both of which combine modern nano-elctronics with machine learning to obtain more insights in 1) disease progress of each patient (Onera or 2) insights in how well patients use inhaler medication (

My passion, however is twofold: First, spending time with patients face to face, for which I continue practicing internal medicine in a privately held sleep clinic in Frankfurt (American Sleep Second, my early independence from academic institution allows me to spend the first five days of each month vacation time with my wife, while the rest of weekends and travel is spent together with friends and business partners in Europe and the US, all of which provide a very rich intellectual learning experience and satisfaction.

  1. Positions and Employment

1988-1996       Sleep Research Fellowship, Sleep Disorders Center and Department of Physiology, Philipps University, Marburg, Germany

1992-2000       Internal Medicine, Philipps University, Marburg, Germany

1996-1999       Pulmonary Postdoctoral Fellowship, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD

1999-present   Assistant Professor (Privatdozent) Philipps University, Marburg, Germany

2001-2003       Research Associate, Johns Hopkins University School of Medicine, Baltimore, MD

2004-2005       Instructor of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

2005-2016       Assistant Professor of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

2016-2018       Associate Professor of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

2009-present   Medical Director of the American Sleep Clinic, Frankfurt

2017-present   Chief Medical Officer and Co-founder of Onera

2018-present   Chief Medical Officer and Co-founder of

Other Experience and Professional Memberships

1992-               Member, German Sleep Society

2000-               Member, American Thoracic Society

2002-               Member, American Professional Sleep Society Honors

2009-               Medical Director, American Sleep Clinic, Frankfurt Germany

2012-               NIH Reviewer, Study Sections of the NHLBI (>10 invitations)

2013-2015       Industry Consultant for Linde (Establishing a Sleep program in Abu Dhabi)

2005-present:  Advisor and Board Member of TNI Medical/Germany, which partnered with Masimo Inc.

2015-present:  Advisor and Consultant for

Contribution to Science

Selected from over 100 publications (Research Gate: +3000 Citations, h-index: 25):

  1. My first research projects focused examining the effect of sleep on patients with Chronic Obstructive Lung disease (COPD) Obstructive sleep apnea (OSA) and coronary artery diseases (CAD). Specifically, I developed methods and techniques that allowed us to perform bedside testing (Ref 1-2) and epidemiologic field studies (Ref 3). In subsequent work, I performed pathophysiologic studies and found that common used sleep medication contributed to increased work of breathing during sleep in normal individuals (Ref 4).  Moreover, I demonstrated that in patients with COPD and CAD, the application of CPAP let to an offloading of breathing loads during sleep (Ref 5-6) potentially through mechanisms that offload the cardiovascular stress of these diseases.
  2. Schneider H, Penzel T, Peter JH. Cardiorespiratory Diagnosis of Sleep Related Breathing Disorders with the Mobile 10 Chanel Unit SIDAS. In: Smirne S, ed. Immunology and Sleep. Milano: Masson, 1993:365-372.
  3. Schneider H. Bestimmung der Atemantwort im Schlaf. In: Peter JH, von Wichert P, eds. Schlaf – Atmung – Kreislauf. Berlin: Springer, 1993:121-133.
  4. Bearpark H, Elliott L, Grunstein R, Cullen S, Schneider H, Althaus W, Sullivan C. Snoring and sleep apnea: A population study in Australian men. Am J Respir Crit Care Med; 151: 1459-1465, 1995.
  5. Schneider H, Grote L, Peter JH, Guilleminault C von Wichert P. Flunitrazepam –Two Benzodiazepines with Different Half-Life on Breathing During Sleep. Chest 109:909-915, 1996.
  6. Schneider H, Becker H, Fus E, Stammnitz E, Peter JH, von Wichert P. Nasale positive Druckbeatmung bei Patienten mit ausgeprägter COPD, Med. Klin. 89, 71-73, 1994.
  7. Schneider H, Janicki J, Stammnitz A, Peter JH. Die kardiorespiratorische Polygraphie zur Differentialdiagnostik der respiratorischen Insuffizienz nach koronarer Bypass Operation. Klin. 92: 104-107, 1997.
  8. The natural progression of my first research experience was to transition into a more focused pathophysiologic approach for determining the mechanisms by which sleep disordered breathing, and mainly OSA, produce hemodynamic changes during sleep. I received a stipend from the German Research Society to further my research at the Johns Hopkins University. I used chronically instrumented dog model of obstructive sleep apnea (OSA) to demonstrate that the acute elevations in systemic and pulmonary pressure during induced airway obstructions are due to exuberant neural responses to hypoxia rather than mechanical effects on the heart. (Ref 7-9). The work concluded a long term dispute, of whether mechanical of neural effects were responsible for the acute hemodynamic changes in OSA.  Moreover, at the end of this series of publications I was established as an astute physiologist and an independent researcher.
  9. Schneider H, Schaub C.D, Andreoni K.A, Schwartz A.R, Smith P.L, Robotham J.L, Donnell C.P. Systemic and pulmonary hemodynamic responses to normal and obstructed breathing during sleep. J. Appl. Physiol. 83(5), 1670-1680, 1997.
  10. Schneider H, Schaub CD, Chen CA, Andreoni KA, Schwartz AR, Smith PL, Robotham JL, and O’Donnell CP. Neural and local effects of hypoxia on cardiovascular responses to obstructive apnea.  J Appl Physiol 88: 1093-1102, 2000.
  11. Schneider H, Schaub CD, Chen CA, Andreoni KA, Schwartz AR, Smith PL, Robotham JL, and O’Donnell CP.  The effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea.  J Appl Physiol 88: 1084-1092, 2000.

3.) After these initial physiologic studies in canine models, I focused on a series of studies in murine models and in humans to find methods how to prevent sleep disordered breathing, rather than studying outcomes.  I was the first to demonstrate that the inspiratory duty cycle, but not the respiratory rate predicts hypoventilation in response to upper airway obstruction and that the inspiratory duty cycle response to hypercapnia has a genetic component that is linked to chromosome 9 in a mouse model (10).  In a subsequent manuscript, he also demonstrated that the inspiratory duty cycle serves as a marker for treatment responses in children with severe upper airway obstruction without sleep apnea (11-13).  In summary, my conceptual approach has broad implications for clinical (genetic-based) research but also direct clinical translational component for managing patients with upper airway obstruction and sleep apnea and general pulmonary diseases such as COPD, asthma and cystic fibrosis (8).

  1. Schneider H, SP Patil, S Canisius, E A Gladmon, AR Schwartz, CP O’Donnell, PL. Smith, and CG. Tankersley Hypercapnic duty cycle is an intermediate physiological phenotype linked to mouse chromosome 5. J Appl Physiol; 285: 11-19, 2003.
  2. Schneider H, Krishnan V, Pichard LE, Patil SP, Smith PL, Schwartz AR. Inspiratory duty cycle responses to flow limitation predict nocturnal hypoventilation. Eur Respir J. 2009 May; 33(5):1068-76, 2009.
  3. Chin CH, Kirkness JP, Patil SP, McGinley BM, Smith PL, Schwartz AR, Schneider H. Compensatory Responses to Upper Airway Obstruction in Obese Apneic Men and Women. J Appl Physiol. 2011 Nov 17, 2011.
  4. Biselli PJ, Grossman PR, Kirkness JP, Patil SP, Smith PL, Schwartz AR, Schneider H. The Effect of Increased Lung Volume in Chronic Obstructive Pulmonary Disease on Upper Airway Obstruction during Sleep. J Appl Physiol (1985) 2015 Aug 1;119(3):266-71

4.) Over the last few years, I developed a novel treatment concept for assisting ventilation during sleep (nasal air insufflations).  This device is now in clinical use and promise to significantly impact the management of children with Sleep Disorders and patients with chronic obstructive pulmonary diseases. My work related to this novel therapy concept was selected in 2010 from the Journal of Sleep: Best in Sleep 2010 (12). I also received an RO1 to compare this novel treatment to conventional oxygen therapy.  During the last two years, I received additional 2 grants, one from the CF Foundation, the other from the National Sleep Foundation, both grants provide the means to obtain the necessary data to transition the current research into larger NIH sponsored multicenter clinical trials in this area.

  1. McGinley B, Halbauer, A, Patil SP, Smith C, Smith PL, Schwartz AR, Schneider H. An Open Nasal Cannula Treats Obstructive Sleep Apnea in Children-.Pediatrics. 2009 Pediatrics. 2009 Jul; 124(1):179-88, 2009.
  2. Paranjape SM; McGinley BM; Braun AT; Schneider H.  Polysomnographic Markers in Children with Cystic Fibrosis Lung Disease. Pediatrics 2015-1747., accepted, August 2015.
  3. McGinley B, Patil SP, DeRosa PA, Kirkness JP, Smith C, Smith PL, Schwartz AR, Schneider H. A novel therapeutic approach for obstructed sleep disordered breathing – treatment with nasal insufflation (TNI). Am J Respir Crit Care Med. 2007 Vol 176, pp 194-200, 2007. Also Selected for Best in Sleep 2010: Sleep 2010
  4. Nilius G, Wessendorf T, Maurer J, Stoohs RA, Patil SP, Schubert N, Schneider H. Predictors for Treating Obstructive Sleep Apnea with an Open Nasal Cannula System (TNI), 2010 Mar; 137(3):521-8, 2010.
  5. Mündel T, Sheng F, Tatkov S, Schneider H. Mechanisms of nasal high flow on ventilation during wakefulness and sleep. J Appl Physiol. 2013 Apr;114(8):1058-65.
  6. Malhotra A, Schwartz AR, Schneider H, Owens RL, DeYoung P, Han MK, Wedzicha JA, Hansel NN, Zeidler MR, Wilson KC, Badr MS; Research Priorities in Pathophysiology for Sleep-disordered Breathing in Patients with Chronic Obstructive Pulmonary Disease. An Official American Thoracic Society Research Statement. ATS Assembly on Sleep and Respiratory Neurobiology. Am J Respir Crit Care Med. 2018 Feb 1
  7. Grote L, Sommermeyer D, Ficker J, Randerath W, Penzel T, Fietze I, Sanner B, Hedner J, Schneider H. REM Sleep Imposes a Vascular Load in COPD Patients Independent of Sleep Apnea. COPD. 2017 Dec;14(6):565-572.
  8. Eskandari D, Zou D, Grote L, Schneider H, Penzel T, Hedner J. Independent associations between arterial bicarbonate, apnea severity and hypertension in obstructive sleep apnea. Respir Res. 2017 Jun 28;18(1):130..
  9. Biselli PJ, Kirkness JP, Grote L, Fricke K, Schwartz AR, Smith P, Schneider H. Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study. J Appl Physiol (1985). 2017 Jan 1;122(1):82-88.
  1. International (2) and US Patents (6):

2000:   Auto CPAP Device: Vorrichtung zur Erfassung der Atmungstaetigkeit: DE000010031079A1,
The technology is also protected PCT 02/00283, DE000010103810.0 PCT02/060518

2001:   Device for Trans-Nasal Insufflation for treating Snoring and mild degrees of upper airway Obstruction “also called Anti Snore device” US 020040016432A1, The technology is also protected WO002002062413A1, WO002002062413A3, DE00001010538C2 EP0000013599671A2,

2006:   Device for detecting the respiratory activity of a person. United States Patent 7,089,936

2006:   Anti-snoring device, method for reducing snoring, and a nasal air cannula United States Patent 7,080,645

2006:   Method and apparatus for detecting the respiratory activity of a person:  United States Patent 7,934,500

2008:   Disposable Sleep and Breathing Monitor: United States Patent  US 2008/0092898

2010    Method and device for carrying out a signal-processing viewing of a measurement signal that is correlated to the respiratory activity of an individual United States Patent 7,722,546

2011:   Apparatus and method for supplying a respiratory gas:  United States Patent 8,061,35



Ongoing Research Support

Research Agreement with Industry Sponsor          Schneider PI                                       1/2017 – 12/2018

Principal Investigator: Hartmut Schneider, M.D., Ph.D.

Role: Principal Investigator, 40% effort.

The purpose of this study is to determine the accuracy of Itamar WatchPat for diagnosing obstructive and central sleep apnea across a spectrum of patients with co-morbidities.

         Selected Past Research Support Relevant For this Application (3 from 6)

R01  HL105546-01                                                  Schneider (PI)                                     07/01/11-05/31/16

Pathogenesis and Outcomes of Sleep Disordered breathing in COPD

The overall goal of this RO1 grant is to study the effect of nasal insufflations on pulmonary function and morning fatigue in COPD.

CF foundation NA_00046790                                  Schneider (Co-PI)                       07/05/13 – 06/31/16

Sleep-Related Ventilatory Mechanics & Energy Expenditure in Children & Adults with Cystic Fibrosis

The purpose of this project is to demonstrate that sleep can be utilized to prevent pulmonary cachexia.

National Sleep Foundation                                       Schneider (Mentor)                      07/01/15-05/30/16

The purpose of this project is to determine if nasal insufflation can alter energy expenditure in
patients with CF

P50 HL084945                                                         Wise (PI)                                          09/14/07-08/31/12

SCCOR:  Mechanisms and Treatment of COPD Progression

Project 3 (PI: Alan R. Schwartz, M.D.): Mechanisms and Impact of Sleep Disordered Breathing in COPD”

The overall goal of this SCCOR program is to understand the complex interplay of mechanisms that promote the progression of COPD and to translate that understanding into treatments that can benefit persons who suffer from COPD. Project III will elucidate the mechanisms and impact of sleep disordered breathing in COPD. Role: Co-Investigator


K23 HL 72126                                                     Schneider (PI)                                  01/2004-12/8/2009

Respiratory Phenotypes of Obstructive Sleep Apnea

The purpose of this project was the characterization of respiratory phenotypes for obstructive sleep apnea.  This grant laid down the foundation for the conceptual approach of the current application and the invention of the SBIR.