Abstract

BackgroundReducing intrathoracic pressure in the setting of compromised cerebral perfusion due to acute brain injury has been associated with reduced intracranial pressure and enhanced cerebral perfusion pressure and blood flow in animals. Noninvasive active intrathoracic pressure regulation lowers intrathoracic pressure, increases preload, reduces the volume of venous blood and cerebral spinal fluid in the skull, and enhances cerebral blood flow. We examined the feasibility of active intrathoracic pressure regulation therapy in patients with brain injury. We hypothesized that active intrathoracic pressure regulation therapy would be associated with lowered intracranial pressure and increased cerebral perfusion pressure in these patients.MethodsAt three institutions, active intrathoracic pressure regulation therapy (CirQlator™, ZOLL) was utilized for 2 consecutive hours in five mechanically ventilated patients with brain injury. A 30-minute interval was used to collect baseline data and determine persistence of effects after device use. End-tidal carbon dioxide was controlled by respiratory rate changes during device use. The intracranial pressure, mean arterial pressure, and cerebral perfusion pressure were recorded at 5-minute intervals throughout all three periods of the protocol. Results for each interval are reported as mean and standard deviation.ResultsIntracranial pressure was decreased in all five patients by an average of 21% during (15 ± 4 mmHg) compared to before active intrathoracic pressure regulation (19 ± 4) (p = 0.005). This effect on intracranial pressure (15 ± 6) was still present in four of the five patients 30 minutes after therapy was discontinued (p = 0.89). As a result, cerebral perfusion pressure was 16% higher during (81 ± 10) compared to before active intrathoracic pressure regulation (70 ± 14) (p = 0.04) and this effect remained present 30 minutes after therapy was discontinued. No adverse events were reported.ConclusionsThese data support the notion that active intrathoracic pressure regulation, in this limited evaluation, can successfully augment cerebral perfusion by lowering intracranial pressure and increasing mean arterial pressure in patients with mild brain injury. The measured effects were immediate on administration of the therapy and persisted to some degree after the therapy was terminated.

Highlights

  • Reducing intrathoracic pressure in the setting of compromised cerebral perfusion due to acute brain injury has been associated with reduced intracranial pressure and enhanced cerebral perfusion pressure and blood flow in animals

  • Cerebral circulation is generally assessed by measuring the cerebral perfusion pressure (CerPP), defined as the difference between the mean arterial blood pressure (MAP) and the intracranial pressure (ICP)

  • Exclusion criteria Patients could not be included if they: had a cardiac or pulmonary injury impacting intrathoracic pressure (ITP) and/or cardiac function; had radiologically evident pneumothorax or hemothorax; had neck injury resulting in neck swelling with jugular venous compression; had ongoing uncontrolled bleeding; had respiratory disease, for example, chronic obstructive pulmonary disease (COPD), interstitial lung disease, or other parenchymal or pulmonary vascular disease; had marked hypertension, which was defined as systolic blood pressure (SBP) > 180 mmHg; had heart failure; had a positive serum or urine pregnancy test or breast feeding for women

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Summary

Introduction

Reducing intrathoracic pressure in the setting of compromised cerebral perfusion due to acute brain injury has been associated with reduced intracranial pressure and enhanced cerebral perfusion pressure and blood flow in animals. Noninvasive active intrathoracic pressure regulation lowers intrathoracic pressure, increases preload, reduces the volume of venous blood and cerebral spinal fluid in the skull, and enhances cerebral blood flow. We examined the feasibility of active intrathoracic pressure regulation therapy in patients with brain injury. We hypothesized that active intrathoracic pressure regulation therapy would be associated with lowered intracranial pressure and increased cerebral perfusion pressure in these patients. Small increases in intracranial volume and the subsequent elevation in intracranial pressure (ICP) that impedes cerebral blood flow (CBF) can be accommodated by the movement of blood and cerebral spinal fluid (CSF) out of the cranium. It has been suggested that CerPP be maintained above 60–70 mmHg to minimize BI and optimize patient survival following brain injury [5, 6]

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