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The relative contribution of hemodynamic parameters to blood pressure decrease in classical orthostatic hypotension

Journal of Hypertension, vol. 43, pp. 436–444

Abstract

PURPOSE: We studied the relative contributions of total peripheral resistance (TPR), stroke volume (SV) and heart rate (HR) to low blood pressure in classical orthostatic hypotension (cOH) on group and individual levels. METHODS: We retrospectively analyzed tilt test records from cOH patients and age/sex-matched controls. We quantified relative effects of HR, SV and TPR on mean arterial pressure (MAP) with the log-ratio method. We studied relations of changes of HR, SV or TPR with the change of MAP across patients and variability of contributions of HR, SV and TPR to MAP. We also explored neurogenic vs. nonneurogenic causes. RESULTS: MAP responded to tilt with a decrease in patients ( n = 80) and an increase in controls ( n = 80). A too small TPR-increase contributed most to cOH, followed by a too large SV-decrease; both effects were partially corrected by a larger increase of HR. Only TPR changes consistently affected MAP change in patients and controls. TPR decreased almost exclusively in patients, most in those with severe cOH. Contributions of HR, SV and TPR to MAP did not differ between probable neurogenic and nonneurogenic causes. CONCLUSION: HR, SV and TPR all contributed to cOH, with a key role for TPR; a decrease of TPR was almost unique to patients and may be due to hyperventilation. The lack of differences between neurogenic and nonneurogenic causes needs further study.

Authors 10

  1. Leiden University · Leiden University Medical Center · Stichting Epilepsie Instellingen Nederland

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

    Stichting Epilepsie Instellingen Nederland-SEIN, Heemstede

  2. Leiden University · Radboud University Nijmegen · Leiden University Medical Center · Radboud University Medical Center

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

    Department of Neurology, Radboud University Medical Centre, Nijmegen, The Netherlands

  3. Lund University · Skåne University Hospital

    Affiliation as printed

    Department of Cardiology, Skåne University Hospital

    Department of Clinical Sciences, Lund University, Malmö, Sweden

  4. Leiden University · Leiden University Medical Center

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

  5. Leiden University · Leiden University Medical Center

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

  6. Leiden University · Leiden University Medical Center

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

  7. Erasmus MC

    Affiliation as printed

    Department of Experimental Cardiology, Erasmus Medical Centre, Rotterdam, The Netherlands

  8. Leiden University · Leiden University Medical Center · Stichting Epilepsie Instellingen Nederland · UCL Queen Square Institute of Neurology · University College London

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

    Stichting Epilepsie Instellingen Nederland-SEIN, Heemstede

    UCL Queen Square Institute of Neurology, University College London, London, UK

  9. Karolinska University Hospital · Lund University · Karolinska Institutet

    Affiliation as printed

    Department of Cardiology, Karolinska University Hospital

    Department of Clinical Sciences, Lund University, Malmö, Sweden

    Department of Medicine, Karolinska Institute, Stockholm, Sweden

  10. Leiden University · Leiden University Medical Center

    Affiliation as printed

    Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden

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References 31