title: [Systolic, diastolic and pulse pressure: pathophysiology].
abstract: Arterial hypertension is the result of abnormal flow/resistance relationships. Resistance to outflow consists of different components: the systolic component is the one generated by conductance vessels, whereas the diastolic component consists of peripheral resistance, which regulates peripheral blood supply due to the run-off of conductance vessels during left ventricular diastole. Thus, an increase in systemic resistance results in a rise in diastolic blood pressure. If the elasticity of conductance vessels decreases, diastolic run-off also decreases and diastolic blood pressure goes down. When this loss of elasticity occurs, the ejection force cannot be anymore offset by arterial distension, the pulse wave velocity increases and reflex waves to the heart arrive earlier, causing the systolic blood pressure to augment. Such an augmentation, together with decreasing diastolic blood pressure results in an enhancement of the pulse pressure. When the stroke volume is normal, an increase in pulse pressure is, therefore, a marker of altered conductance. However, if, due to loss of elasticity of the conductance arteries diastolic blood pressure goes down, increasing systolic pressure also protects against a decrease in mean pressure. Indeed, in conditions of elevated pulse pressure, the mean pressure can be normal or high, indicating that when evaluating blood pressure all components should be taken into consideration. A high systolic blood pressure associated with a normal mean blood pressure is suggestive of a normal peripheral resistance. In this context, isolated systolic hypertension can be conveniently divided into a normal peripheral resistance type, and into a high peripheral resistance type when it is associated with high values of mean blood pressure (independently of whether or not the diastolic blood pressure is increased). In this latter occurrence, a high pulse pressure is more likely to be a marker of severe target organ damage (conductance arteries) than of a direct causal risk factor such as systolic blood pressure.
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università degli Studi Federico II, Napoli. simogi@unina.it
authors.forename: G
authors.initials: G
authors.lastname: de Simone
authors.forename: F
authors.initials: F
authors.lastname: Pasanisi
mesh_terms: D001794:Blood Pressure; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*