B E Smith1, V M Madigan2. 1. School of Medicine, University of Notre Dame, Australia, Darlinghurst, NSW, 2010, Australia. brendanprivate@hotmail.com. 2. School of Biomedical Science, Charles Sturt University, Bathurst, NSW, 2795, Australia.
Abstract
PURPOSE OF REVIEW: This article introduces the haemodynamic principles that underpin the pathophysiology of hypertension and introduces a rational physiological approach to appropriate pharmacologic treatment. RECENT FINDINGS: Outdated understanding of haemodynamics based on previous measurement systems can no longer be applied to our understanding of the circulation. We question the current view of hypertension as defined by a predominantly systolic blood pressure and introduce the concept of vasogenic, cardiogenic and mixed-origin hypertension. We postulate that failure to identify the individual's haemodynamic pattern may lead to the use of inappropriate medication, which in turn may be a major factor in patient non-compliance with therapeutic strategies. A population-based approach to treatment of hypertension may lead to suboptimal functional dynamics in the individual patient. Finally, we question the validity of current guidelines and published evidence relating morbidity and mortality to the future treatment of hypertension. The importance of individual haemodynamic profiles may be pivotal in the understanding, diagnosis and treatment of hypertension if optimal control with minimal adverse effects is to be achieved. Research based on individual haemodynamic patterns is overdue.
PURPOSE OF REVIEW: This article introduces the haemodynamic principles that underpin the pathophysiology of hypertension and introduces a rational physiological approach to appropriate pharmacologic treatment. RECENT FINDINGS: Outdated understanding of haemodynamics based on previous measurement systems can no longer be applied to our understanding of the circulation. We question the current view of hypertension as defined by a predominantly systolic blood pressure and introduce the concept of vasogenic, cardiogenic and mixed-origin hypertension. We postulate that failure to identify the individual's haemodynamic pattern may lead to the use of inappropriate medication, which in turn may be a major factor in patient non-compliance with therapeutic strategies. A population-based approach to treatment of hypertension may lead to suboptimal functional dynamics in the individual patient. Finally, we question the validity of current guidelines and published evidence relating morbidity and mortality to the future treatment of hypertension. The importance of individual haemodynamic profiles may be pivotal in the understanding, diagnosis and treatment of hypertension if optimal control with minimal adverse effects is to be achieved. Research based on individual haemodynamic patterns is overdue.
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