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Cerebral Monitoring May Aid Assessment of Brain Function During Cardiac Arrest

The overall aims of neuromonitoring are to identify worsening neurological function and secondary cerebral insults that may benefit from specific treatment(s) and improve pathophysiological understanding of cerebral disease in critical illness, to provide clear physiological data to guide and individualize therapy, as well as assist with neuroprognostication. It’s not a novel concept to directly monitor the organ of interest to direct and assess therapies.

The human brain constitutes 2% of the total body weight, yet the energy-consuming processes that enable the brain to function adequately account for about 25% of total body energy expenditure and 20% oxygen consumption of the whole organism.

Noninvasive evaluation of cerebral blood flow (CBF) is possible with transcranial Doppler (TCD), utilizing derived pulsatility index or optic nerve sonography. However, methods for continuous online monitoring of the brain remains primarily invasive.

Intraventricular devices have long been considered the gold standard for measurement of cerebral oxygenation; intraparenchymal devices are particularly useful when intracranial pressure monitoring and drainage is also desirable. Though noninvasive monitoring of cerebral oxygenation exists, there’s little evidence for its usefulness outside of the operating room.

Continuous measurement of CBF is now feasible using a thermal diffusion probe (TDP), which shows good correlation with CBF as measured by xenon-CT.

TCD shows flow velocity rather than flow itself. It combines ultrasound and the Doppler principle to represent erythrocyte flow in the basal cerebral arteries.

As cerebrovascular resistance increases, systolic velocity increases and diastolic velocity decreases. TCD is also used to assess cerebrovascular autoregulation in traumatic brain injury (TBI) and subarachnoid hemorrhage patients. The quality of TCD signal is operator-dependent and correct interpretation requires training. In approximately 10% of patients, transtemporal sonication isn’t feasible.

Brain Tissue Oxygen Monitoring

Arterio-jugular difference in oxygen content (AJDO2), calculated by the arterial minus the jugular bulb venous pressure, is proportional to CBF and inversely proportional to oxygen consumption (i.e., cerebral metabolic rate for oxygen, CMRO2). Normal values for jugular bulb oxygen saturation (SjO2) are about 57% (95% confidence interval 52–62%). This is a global measure and insensitive to small regional changes, and a larger volume of the brain must be under-perfused for a significant abnormality to be detected.

Use of intraparenchymal tissue oxygenation probes (i.e., PbO2 monitors) involves insertion of a probe into the white matter of the brain and provides a reasonable estimate of global brain oxygenation. However, this isn’t a “surrogate” for ischemia. It varies not only with CBF, but also with changes in arterial oxygen tension.

With brain tissue oxygenation (PbtO2), xenon-enhanced CT scanning and SPECT, threshold values vary slightly, depending on what type of PbtO2 monitor is used, but values < 20 mmHg should be treated. The quantity, duration and intensity of brain hypoxic episodes (PbtO2 < 15 mmHg) and any PbtO2 values ≤ 5mmHg are associated with poor outcomes after TBI.

Near infrared spectroscopy utilizes the property that oxyhemoglobin, deoxyhemoglobin and oxidized cytochrome oxidase absorb specific portions of the light spectra. This is correlated to the relative proportions of oxyhemoglobin and deoxyhemoglobin (HbO2/Hb) and oxidized cytochrome oxidase in the tissue. This is made noninvasively and works continuously. However, baseline normal values vary widely, and extracranial contamination is a problem.

Cerebral oximetry is noninvasive and utilizes near-infrared light. It shows regional oxygen saturation (rSO2) of primarily the frontal lobes and provides a measure of cellular O2 extraction, similar to central venous O2 saturation. This modality doesn’t require a pulse wave and has a strong correlation with cerebral blood flow and jugular vein bulb saturation. (See Figure 1.)

Microdialysis, in clinical practice, reveals a pattern of elevated lactate/pyruvate ration, and low glucose is considered as a warning sign for cerebral ischemia/hypoxia. Microdialysis has been used to identify the “optimal” threshold for blood glucose during insulin therapy. However, changes in biomarkers are often too delayed and too variable for widespread clinical utility.

Electrophysiological measurements such as an electroencephalogram (EEG) can be used to detect and manage seizures, as well as is aid in neuroprognostication. Seizures in brain injury are often non-convulsive in nature and increase brain injury if left untreated. Quantitative EEG (qEEG) utilizes algorithmic recognition of EEG waveforms and may also be used to monitor the depth of sedation in the ICU.

The most commonly used modality is the bispectral index (BIS) that ranges from 0 (brain dead) to 100 (normal brain function); a value of < 60 indicates general anesthesia and < 30 indicates burst suppression.

For neuroprognostication, somatosensory evoked potentials (SSEPs) are less affected by pharmacological agents or hypothermia than the EEG. This usually occurs at 20 millisecond after the stimulus, and hence is called the N20 peaks. Of the N20, SSEP is highly associated with persistent vegetative state or death in patients.

Integration of Variables

A single monitoring technique may not fully describe the complex pathophysiological changes in the brain, and the concept of multimodality monitoring—the simultaneous digital recording of multiple parameters of brain functions—has been recommended to use for treatment and prognostication.

ATACH-2 was a clinical trial that randomized patients to set blood pressures goals without directly monitoring the effects on the brain. The study showed no differences in mortality or morbidity in patients receiving intensive blood pressure control compared to standard blood pressure control.1

However, BOOST-2 randomized patients to either ICP monitoring alone or ICP and PbO2 measurements to drive therapy in TBI. In this study, brain tissue oxygenation monitoring reduced brain tissue hypoxia with a trend toward lower mortality and more favorable outcomes than ICP-only treatment.2


Monitoring of brain function should be considered in all comatose patients in the ICU. The goals of neuromonitoring are to identify worsening neurological function and secondary insults that may benefit from specific treatments, to improve pathophysiological understanding of cerebral disease in critical illness, provide physiological data to guide and individualize therapy, and assist in prognostication.

At present, there’s no “ideal,” single brain monitor, and a combination of monitoring techniques may provide better insight into brain function than a single monitor used alone. Trends over time and threshold values are both important when assessing brain function.

Clinical studies suggest the physiological feasibility and biological plausibility of management based on information from various monitors, but data supporting this concept from randomized trials are still required.

To treat in the ED, first be aware of the most important organ in the body. Secondly, do no harm (i.e., no hypoxia, no hypotension, no hypoglycemia). Be smart about CerPP as autoregulation is shifted in chronic hypertension and may be lost. Therefore, CerPP is dependent on mean arterial pressure. If and when you’re able to monitor, trend and react to oxygenation and flow.


1. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive blood-pressure lowering in patients with acute cerebral hemorrhage. N Engl J Med. 2016;375(11):1033–1043.

2. Okonkwo DO, Shutter LA, Moore C, et al. Brain oxygen optimization in severe traumatic brain injury phase-II: A phase II randomized trial. Crit Care Med. 2017;45(11):1907–1914.