Cerebral Pulsatility Index Is Elevated in Patients with Elevated Right Atrial Pressure

Abstract

BACKGROUND AND PURPOSE:Extracerebral venous congestion can precipitate intracranial hypertension due to obstruction of cerebral blood outflow. Conditions that increase right atrial pressure, such as hypervolemia, are thought to increase resistance to jugular venous outflow and contribute to cerebro-venous congestion. Cerebral pulsatility index (CPI) is considered a surrogate marker of distal cerebrovascular resistance and is elevated with intracranial hypertension. Thus, we sought to test the hypothesis that elevated right atrial pressure is associated with increased CPI compared to normal right atrial pressure. METHODS:We retrospectively reviewed 61 consecutive patients with subarachnoid hemorrhage. We calculated CPI from transcranial Doppler studies and correlated these with echocardiographic measures of right atrial pressure. CPIs were compared from patients with elevated and normal right atrial pressure. RESULTS:There was a significant difference between CPI obtained from all patients with elevated right atrial pressure compared to those with normal right atrial pressure (P < .0001). This finding was consistent in sensitivity analysis that compared right and left hemispheric CPI from patients with both elevated and normal right atrial pressure. CONCLUSION:Patients with elevated right atrial pressure had significantly higher CPI compared to patients with normal right atrial pressure. These findings suggest that cerebro-venous congestion due to impaired jugular venous outflow may increase distal cerebrovascular resistance as measured by CPI. Since elevated CPI is associated with poor outcome in numerous neurological conditions, future studies are needed to elucidate the significance of these results in other populations.

Patient management algorithm combining processed electroencephalographic monitoring with cerebral and somatic near-infrared spectroscopy: a case series

“…1,5 In this particular situation, a reduction in diastolic arterial blood flow velocities secondary to the increase in cerebral venous pressure resulted in a reduction of the PI. 13,14 These changes are similar to those seen in situations associated with intracranial hypertension. 15 The anastomotic stenosis was thought to be secondary to edema of the surrounding tissues.…”

Left ventricular ejection fraction and right atrial diameter are associated with deep regional CBF in arteriosclerotic cerebral small vessel disease

“…It has been confirmed that right atrium enlargement is usually in parallel with elevated right atrial pressure [27]. Moreover, elevated right atrial pressure indicates increased cerebrovascular resistance and cerebrovenous congestion [28]. It is supposed that dilated right atrium may indirectly reflect elevated right atrial pressure which impedes efflux of glymphatic drainage from PVS.…”

A proposed algorithm for combining transcranial Doppler ultrasound monitoring with cerebral and somatic oximetry: a case report

“…Cerebral hypoperfusion would be suspected if mean, systolic, and diastolic cerebral blood velocities of the middle cerebral artery are reduced as opposed to venous congestion where only diastolic cerebral blood velocities will be attenuated with the systolic values remaining unchanged. 14 During venous congestion and elevation in central venous pressure, diastolic cerebral blood velocity from TCD will be reduced and the pulsatility index ([systolic velocities -diastolic velocities]/mean velocities) (normal: 0.81-0.97) increased, 10,15 with reductions in both cerebral and somatic NIRS values. Similar signals will be observed 16 although somatic NIRS values would remain normal.…”

“…An increase in PI can be associated with elevated intracranial pressure (ICP) or with elevation of the central venous pressure. [14][15][16]25,26 Global somatic desaturation will be present if the reduced TCD diastolic velocity and elevated PI is secondary to venous congestion. Nevertheless, global somatic saturation will be normal or maintained if the mechanism of brain desaturation, reduced TCD diastolic velocity, and elevated PI is secondary to intracranial hypertension.…”