Respiratory-related arterial pressure variability as an indicator of graded blood loss: involvement of the autonomic nervous system

Abstract

During positive pressure mechanical ventilation, percentile systolic pressure variation (%SPV) or respiratory-related arterial pressure variability (RAPV) have both been used in assessment of graded haemorrhage. We aimed to investigate whether changes in %SPV and RAPV are correlated during graded haemorrhage (by 5, 10 or 20% of the estimated blood volume) in anaesthetized positive pressure ventilated rats and to investigate the involvement of autonomic regulation. Saline vehicle or atropine produced no discernible effect on baseline %SPV or RAPV but, thereafter, %SPV and RAPV increased progressively with graded haemorrhage. Propranolol significantly decreased baseline %SPV and RAPV and changes induced in %SPV and RAPV by graded haemorrhage. Phentolamine significantly enhanced baseline %SPV and RAPV, and further enhancement of %SPV and RAPV by graded haemorrhage did not occur until 20% of the estimated blood volume was removed. RAPV was significantly correlated with %SPV in all experimental groups. We conclude that RAPV is comparable with%SPV as an indicator of graded haemorrhage and that, in anaesthetized and positive pressure ventilated rats, both are dependent on autonomic function, especially beta-adrenoceptors.

Fluid responsiveness predicted by elevation of PEEP in patients with septic shock

“…7,8 Instead, dynamic haemodynamic measurements during positive pressure ventilation, systolic pressure variation (SPV), stroke volume variation (SVV), and PPV, have been reported to better predict fluid responsiveness. 10,14,[27][28][29] In addition, changes in aortic blood flow velocity and VTI Ao by pulse-Doppler echocardiography and collapse of the superior vena cava or the inferior vena cava have been found to be predictors of fluid responsiveness during mechanical ventilation. 23,24,[30][31][32] These dynamic methods are quite accurate in controlled situations but may have several limitations in clinical practice.…”

Frequency components of systolic blood pressure variability reflect vasomotor and cardiac sympathetic functions in conscious rats

“…Experiments under various physical conditions including external stimuli are thus necessary to make MF more applicable. The mechanism underlying HF has not been adequately explained despite several studies indicating that it is a mechanical consequence of respiration [12, 13] and other studies suggesting an association between HF and ANS, particularly the β-adrenergic system [14–16]. To make progress in the availability of SBPV frequency analysis for the evaluation of sympathetic cardiovascular function, the association between the sympathetic nervous system and SBPV must be determined.…”

“…Most studies of the involvement of sympathetic cardiovascular function in SBPV (particularly in respiratory HF) are conducted under anesthesia [14–16]; therefore, little is known concerning the natural responses to stimuli under unanesthesia when ANS is not suppressed. It is meaningful to examine the ANS response in a conscious state in order to evaluate complicated pathological conditions (e.g., chronic pain) in human [17] and animal models [18–20].…”

Time course of cardiovascular neural regulation during programmed 20-sec apnea in rats

“…Later studies (22,23) demonstrated that the BHFn provides a valid assessment of cardiac sympathetic regulations in anesthetized and ventilated rats. A recent study by Lai and coworkers (27) also showed that the BHFn is an indicator of graded hemorrhage and is dependent on autonomic function, especially cardiac sympathetic functions. The present study further elucidates that the BHFn increases significantly within 6 secs after reventilation and that the increase is attenuated by ␣-adrenergic, ␤-adrenergic, and muscarinic blockades.…”

“…Power of the low-frequency component (BLF), normalization high-frequency component (BHFn) of the SAP spectrogram, and highfrequency component (HHF) of the interbeat spectrogram were quantified (19,21,22). BHFn, BLF, and HF provided markers of cardiac sympathetic modulation (18,22,23,27), sympathetic vasomotor activity (19, 29 -33), and cardiac vagal activity (30,31,34,35), respectively.…”