Acute hypoxia diminishes the relationship between blood pressure and subarachnoid space width oscillations at the human cardiac frequency.

BACKGROUND:Acute hypoxia exerts strong effects on the cardiovascular system. Heart-generated pulsatile cerebrospinal fluid motion is recognised as a key factor ensuring brain homeostasis. We aimed to assess changes in heart-generated coupling between blood pressure (BP) and subarachnoid space width (SAS) oscillations during hypoxic exposure. METHODS:Twenty participants were subjected to a controlled decrease in oxygen saturation (SaO2 = 80%) for five minutes. BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography, oxyhaemoglobin saturation with an ear-clip sensor, end-tidal CO2 with a gas analyser, and cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a recently-developed method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between BP and SAS oscillations. RESULTS:Gradual increases in systolic, diastolic BP and HR were observed immediately after the initiation of hypoxic challenge (at fifth minute +20.1%, +10.2%, +16.5% vs. baseline, respectively; all P<0.01), whereas SAS remained intact (P = NS). Concurrently, the CBFV was stable throughout the procedure, with the only increase observed in the last two minutes of deoxygenation (at the fifth minute +6.8% vs. baseline, P<0.05). The cardiac contribution to the relationship between BP and SAS oscillations diminished immediately after exposure to hypoxia (at the fifth minute, right hemisphere -27.7% and left hemisphere -26.3% vs. baseline; both P<0.05). Wavelet phase coherence did not change throughout the experiment (P = NS). CONCLUSIONS:Cerebral haemodynamics seem to be relatively stable during short exposure to normobaric hypoxia. Hypoxia attenuates heart-generated BP SAS coupling

Doppler indexes of left ventricular systolic and diastolic function in relation to the arterial stiffness in a general population

Late-systolic loading of the left ventricular (LV) is determined by arterial wave reflections and central vascular stiffening. We, therefore, investigated the relationship between various Doppler indexes reflecting LV systolic and diastolic function and arterial stiffness in the framework of a large population study of randomly recruited study participants.status: publishe

Doppler indexes of left ventricular systolic and diastolic function in relation to the arterial stiffness in a general population

BACKGROUND: Late-systolic loading of the left ventricular (LV) is determined by arterial wave reflections and central vascular stiffening. We, therefore, investigated the relationship between various Doppler indexes reflecting LV systolic and diastolic function and arterial stiffness in the framework of a large population study of randomly recruited study participants. METHODS: In 1233 study participants (51.7% women; mean age, 48 years; 41.5% hypertensive), using conventional and tissue Doppler imaging, we measured: the transmitral early (E) and late (A) diastolic velocities; tissue Doppler imaging systolic and early (e') and late diastolic mitral annular velocities; and end-systolic longitudinal and radial strain. Using applanation tonometry, we assessed central pulse pressure (cPP), augmentation pressure and carotid-femoral pulse wave velocity. RESULTS: After full adjustment, transmitral E and A peaks increased with augmentation pressure and cPP (P less than 0.0001) and e' was positively associated with cPP (P\u200a=\u200a0.013). The E/e' ratio increased significantly with augmentation pressure (P less than 0.0001), cPP (P less than 0.0001) and pulse wave velocity (P\u200a=\u200a0.048). Although accounting for covariables, all arterial indexes were on average significantly higher in the diastolic dysfunction group with elevated filling pressure (n\u200a=\u200a171) when compared to participants with normal diastolic function (n\u200a=\u200a961; P\u200a 64\u200a0.0004) or with impaired relaxation (n\u200a=\u200a101; P\u200a 64\u200a0.008). Longitudinal strain decreased independently with mean arterial pressure (P\u200a=\u200a0.03). The correlation between radial strain and the arterial indexes shifted from positive at middle age (50-60 years) to negative at older (P less than 0.0001 for interaction). CONCLUSION: Our study underscored the importance of arterial characteristics as a mediator of LV systolic and diastolic dysfunction. We demonstrated an age-dependent relationship between radial strain and indexes of arterial stiffness. Comment in Indices of central aortic pressure waveform and ventricular function: an intimate conversation changing direction with age. [J Hypertens. 2016

Effects of 60 s Mueller manoeuvres series on SAS, SBP, DBP, HR, CBFV, PI, RI and SaO₂.

<p>Data are presented as mean values and standard deviations (SD). All % changes are calculated with reference to baseline values.</p

Characteristics of the study participants.

<p>Data are presented as mean values and standard deviations (SD).</p

Representative tracings of 10 s signals of baseline (in green), 10 s of minimum WCO (in blue) and 10 s of maximum WCO (in red).

<p>BP oscillations (panel A), SAS oscillations (panel B) and WCO (panels C, D and E). Cardiac frequency is indicated by vertical, magenta, dotted lines. Black solid lines (panels from C to E) illustrate results obtained for IAAFT surrogates.</p

Increased inspiratory resistance affects the dynamic relationship between blood pressure changes and subarachnoid space width oscillations - Fig 4

<p>Representative WCO (panel B) and WPCO (panel C) tracings. BP (red) and SAS (blue) signals are provided in the panel A. WCO reaches its minimum between 8 and 18 s of the Mueller manoeuvres, and later upon recovery, reaches its maximum between 35 and 45 s for cardiac frequency. WPCO remains stable. Cardiac frequency is indicated by horizontal dotted lines.</p