Hospice & Palliative Medicine International Journal

Narrative Review Open Access

Multimodal cerebral perfusion monitoring, use at

the patient’s bedside
Abstract Volume 7 Issue 4 - 2024
The human brain is the organ that consumes the most oxygen in the basal state, when
presenting a decrease in oxygen supply, physiological mechanisms are activated to preserve
María Camila Valencia Mendoza,1 Dormar
this supply and thus avoid permanent brain injuries. When a brain injury of any cause David Barrios Martínez2,3,4,5
1
Neurology Resident Physician, Department of Neurology,
occurs, it is essential to carry out a correct diagnosis and monitoring, to establish early and
Hospital Universitario La Cardio, Bogotá, Colombia
effective therapeutic actions to reduce secondary organic damage, seeking to improve the 2
Academic Coordinator Adult Intensive Care Unit, MSc
prognosis of patients with severe neurological injuries. Next, a review of the physiology Education for Health Professionals, Department of Critical
of cerebral metabolism and multimodal perfusion monitoring techniques, measurement of Medicine and Intensive Care, Hospital Universitario San Vicente
cerebral metabolism and its correct interpretation is carried out. Fundación, Medellín, Colombia
3
Medical Specialist in Critical Medicine & Intensive Care,
Keywords: brain, brain metabolism, brain monitoring, neurocritical care, neuroprotection Department of Critical Medicine and Intensive Care, Hospital
General de Medellin, Medellín, Colombia
4
Medical Specialist in Critical Medicine & Intensive Care,
Department of Critical Medicine and Intensive Care, Clínica
Angiosur, Medellín, Colombia
5
Professor, Universidad CES, Colombia

Correspondence: Dormar David Barrios Martínez, Academic

Coordinator Adult Intensive Care Unit, MSc Education for
Health Professionals, Department of Critical Medicine and
Intensive Care, Hospital Universitario San Vicente Fundación,
Medellín, Colombia, Email

Received: December 02, 2024 | Published: December 13,

2024

Introduction tasks at the brain level and how it has systemic repercussions in the
face of brain dysfunction; how this irregular behavior leads to multiple
From a metabolic point of view, the brain is the most oxygen- disorders and its multi-organ effect. In order to know the current status
consuming organ in the human body. The human brain accounts for of this topic, a narrative review was carried out, aimed at finding
2% of body weight and uses 15-20% of cardiac output and consumes out different techniques to perform multimodal cerebral perfusion
approximately 20% of total body oxygen and 25% of all glucose.1,2 monitoring, indications, devices and current implications. The relevant
The neuron, the main cell of the nervous system, is more than 90% terms or keywords used to perform the bibliographic searches were:
dependent on oxygen for ATP production and almost exclusively Brain, Brain metabolism, Brain monitoring, Neurocritical care, Neuro
dependent on oxygen to generate energy from glucose. Its consumption protection, Brain, Brain metabolism, Brain monitoring, Neurocritical
in healthy people is approximately 3.5 ml/100g tissue/min. Of this, care, Neuroprotection. These terms are referred to as free language,
only about one third of the oxygen is consumed since it also has a and the MeSH platform was used to translate them into controlled
large reserve capacity.1 Oxygen demands are directly proportional to language. The following databases were used to conduct the narrative
the neuronal metabolic rate. Oxygen is entirely used for mitochondrial review: PubMed, Embase, Google Scholar, Scielo, Cochrane. Part of
oxidation of glucose in order to generate energy.1,3
the search was limited to text articles only (Table 1).4
Methodology
A detailed review of how oxygen is involved in multiple metabolic
Table 1 Methodology

Inclusion and exclusion criteria

Items Inclusion Criteria Exclusion Criteria
Language English & Spanish Different languages
Seniority Maximum 10 years More than 10 years
Thematic Narrative Reviews, Sysematic Reviews, Meta-analyses and Clinical Practice Guidelines Articles different from the inclusion criteria
The recommendations of the Scale for the Assessment of Narrative Review Articles -
Quality Guidelines other than inclusion criteria
SANRA(25) were followed
Brain, Brain metabolism, Brain monitoring, Neurocritical care, Neuroprotection, Brain,
MeSH terms Terms different from the inclusion criteria
Brain metabolism, Brain monitoring, Neurocritical care, Neuroprotection

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Brain physiology position and negative in the standing position.1,11 To maintain constant
ICP, any variation in the volume of any of the compartments must
When we talk about the functional and structural organization of be counter-regulated by the others. When this mechanism fails, ICP
the central nervous system we must know that it has three components: increases. CSF contributes significantly to ICP regulation in the acute
neurons, supporting tissues or glia and blood vessels. Neurons are phase, mainly through the pressure gradient in the dural venous sinus,
maintained from birth and have a particular characteristic, “they which is responsible for 90% of the increase in ICP, while changes
cannot reproduce when damaged or destroyed”.1 in CSF production and resistance in transit or absorption do not
According to their function, there are three types of cells at the have a major influence on ICP levels.1,11 Cerebral blood flow (CBF)
brain level:1 is about 55 ml/100 g of brain tissue per minute, which corresponds
to approximately 15% of the entire cardiac output. FSC is higher in
- Afferent or sensitive neurons: transform external stimuli from gray matter (78 ml/100g/min) compared to white matter (18 ml/100g/
the environment into a motor and electrical reflex, which can occur min).5
involuntarily (e.g., breathing).
According to the Hagen-Poiseuille equation, laminar flow through
- Efferent or motor neurons: propagate nerve impulses from the a blood vessel is proportional to the pressure difference between the
central nervous system to effector tissues such as muscles and glands. inlet and outlet of the circuit and to the vessel diameter, and inversely
- Multipolar neurons or interneurons: interconnect afferent and proportional to the viscosity of the circulating fluid.12
efferent neurons within neural pathways. Flow = ( ∆P × r 4 ) / ( 8 × n ×1)

Cerebrospinal fluid This pressure gradient is obtained by calculating the difference

between the mean arterial pressure and the venous pressure; this is
A major component in brain physiology is cerebrospinal fluid called the cerebral perfusion pressure. As venous pressure is difficult
(CSF), which bathes the brain parenchyma. It has a volume of to measure, intracranial pressure is measured instead.1
approximately 150 ml with a daily production of approximately 500
ml at a rate of approximately 0.35 ml/minute, two-thirds of which PPC = PAM - PIC
is produced by the choroid plexuses and one-third by the arachnoid Cerebral blood vessels have the intrinsic capacity to maintain a
membranes.5 Experimental biomodels suggest that cerebrospinal fluid constant cerebral flow, in a cerebral perfusion pressure range between
production remains stable if cerebral perfusion pressure is maintained 50 - 150 mmHg, this is known as cerebral autoregulation. Cerebral
between 50-60 mmHg (CPP = MAT - ICP) (Cerebral perfusion autoregulation originates from the resistance of the arterioles which
pressure: CPP; Mean arterial pressure: MAT; Intracranial pressure: adapt their diameter in relation to different stimuli, thus determining
ICP).1 Normal CSF pressure is between 70-180 mmH2O, with an cerebral vascular resistance. When CPP increases above 50 mmHg,
average of 130 mmH2O; which is equal to 10 mmHg in the horizontal cerebral arterioles begin to contract, and cerebral vascular resistance
position.6 The functions of CSF are diverse. As it has the same density begins to increase in order to maintain a constant cerebral flow.
as the brain, it allows the brain to float, maintaining a weight of 50 Conversely, when cerebral perfusion pressure decreases, cerebral
grams. It also helps protect against direct or indirect impact and keeps vascular resistance decreases due to vasodilatation (Figure 1).1,12,13
the brain stable during changes in position, respiration or fluctuations Under pathological conditions this mechanism is compromised and
in blood pressure. On the other hand, it allows the transport of takes a linear trend, as mean arterial pressure falls, cerebral blood
substances such as neurotransmitters, hormones and ions, maintaining flow decreases and as mean arterial pressure rises, cerebral blood flow
the ionic balance within the CNS.1 The CSF also helps to eliminate increases. This means that cerebral blood flow depends on the control
fluids, proteins, cells and metabolic waste production, however, the of the tone of cerebral arterioles, which are modulated by cerebral
glymphatic system has recently been described as a mechanism for perfusion pressure.5 There are also metabolic factors that intervene
promoting the efficient elimination of soluble proteins and metabolites in the regulation of cerebral perfusion pressure, among these are
from the central nervous system and also facilitating the distribution acidosis and tissue hypoxia that cause cerebral vasodilatation and
throughout the brain of various compounds, including glucose, lipids, therefore increase cerebral blood flow, which ultimately leads to
amino acids, growth factors and neuromodulators.7,8 Water transport greater intracranial hypertension.1,11,12,14,15 Another mechanism of great
is regulated by specific proteins called “aquaporins” (AQP). In CSF, importance is the regulation of arterial vessels by partial pressure of
sodium is the main cation and its concentration is similar to that of CO2, where for every 1 mmHg change in paCO2, cerebral blood
plasma. On the contrary, chlorine is found at higher concentrations in volume increases 0.04 ml/100 g of brain tissue.1,11
plasma due to the impermeability of the BBB which is conditioned
by the Donnan effect which speaks of the equilibrium that occurs
between ions when crossing the membrane that will depend on the
concentrations of these and their charges.9 On the other hand, glucose
is transported by diffusion facilitated by the GLUT transport system,
its concentration is equal to 60% of that of plasma.1,3,10

Intracranial pressure and cerebral blood flow

The Monro-Kellie model describes intracranial pressure (ICP)
as the sum of the pressures produced by the volume of the brain
parenchyma, cerebrospinal fluid and blood contained within the veins
and arteries, the latter two remaining constant values. Normal values
will vary with age, changes in body position and clinical situation. In
Figure 1 Brain Autoregulation Curve1
healthy people the normal ICP value is 7-15 mmHg in the horizontal

Citation: Mendoza MCV, Martínez DDB. Multimodal cerebral perfusion monitoring, use at the patient’s bedside. Hos Pal Med Int Jnl. 2024;7(4):136‒141.
DOI: 10.15406/hpmij.2024.07.00258
 Copyright:
Multimodal cerebral perfusion monitoring, use at the patient’s bedside ©2024 Mendoza et al. 138

Among the different factors that contribute to increased or

decreased cerebral blood flow are:1
● CO2: Changes in CO2 levels are closely related to pH. When
CO2 increases, the environment becomes acidic, which causes
arterial dilation and increases cerebral blood flow.
● Potassium: increased potassium levels are a potent vasodilator.
● Adenosine: product of ATP degradation, which causes
vasodilatation and is closely related to the time of tissue hypoxia.
● Nitric oxide: potent vasodilator which is expressed in the cerebral
vascular endothelium by nitric oxide synthase enzymes.
● Prostaglandins: like prostacyclins, they are potent endogenous
vasodilators, which are found to be elevated by measurements
in cerebrospinal fluid of animal models during episodes of
hypotension.
Figure 3 Pressure/volume curve.1
Intracerebral pressure Compliance = ΔV/ΔP
The ICP curve has three peaks in its morphology (Figure 2).1 The
first peak reflects the intracranial inflow of arterial flow, while the other Primary and secondary damage
two are a reflection of venous flow. The first is called the percussion Primary damage is that which occurs during the first hours of the
wave (P1), which has a large, broad, well-defined peak and represents injury, regardless of the cause (ischemia, hemorrhage, trauma, etc.);
the arterial pulse over the choroid plexuses and reflects cerebral flow. from the cellular point of view, structural and functional alterations
The second peak is the plateau or tidal wave (P2) and its amplitude is develop, which can be reversible and irreversible, as well as diffuse
variable but less than P1 and the third peak, also known as the dicrotic or focal. Microscopically, lacerations and retractions of axons are
wave (P3), these last two waves reflect the retrograde venous beat observed, where axonal injury is the common denominator of diffuse
of the jugular veins over the cortical veins. It is important to know cerebral damage; rupture of the cerebral vasculature can also be
that, although the absolute value in the monitor is not modified, it is observed.1,3,10–12,15 Secondary damage refers to additional damage
always necessary to evaluate the morphology of the waves, because it caused by new insults that aggravate or perpetuate the initial primary
can happen that the morphology shows an increase in P2 greater than damage. Its causes may be intracranial or systemic. They can be
P1 and P3 (pyramidal shape) which speaks of venous hypertension, observed at any moment of the patient’s clinical evolution. When they
without representing changes in the absolute value of ICP, which appear, the first thing to do is to treat the primary lesion; however,
alludes to a decrease in compliance.1,12 their prevention, detection and early treatment is essential (Table 2).1
Table 2 Causes of secondary damage16

Systemic Intracranial
Arterial hypotension Intracranial hypotension
Hypoxemia Late cerebral hematoma
Hypercapnia Cerebral edema
Hypocapnia Cerebral hyperemia
Fever Vasospasm
Hyponatremia Seizures
Hypoglycemia
Hyperglycemia
Severe anemia
Figure 2 Intracranial pressure. 1 Acidosis
Disseminated intravascular coagulation
Brain compliance (pressure/volume curve)
Systemic inflammatory response syndrome
The relationship between volume and pressure in the brain is not
linear, which means that in physiological situations brain volume It is also important to recognize the presence of cerebral edema,
can vary without causing alterations in ICP, thanks to compensatory differentiating between vasogenic and cytotoxic cerebral edema.
mechanisms such as those mentioned above; however, after reaching With respect to the former, it occurs when the BBB is disrupted, with
its maximum capacity for autoregulation, ICP increases exponentially. subsequent accumulation of extracellular protein fluids, leading to the
In pathological situations any minimal increase in intracranial release of proinflammatory cytokines and the subsequent infiltration
volume leads to exaggerated increases in intracranial pressure. All of inflammatory cells. Cytotoxic brain edema occurs in the face of
this is explained by the compliance formula that also applies to the dysfunction of ion channels and osmotic flow. With subsequent loss of
intracranial space (Figure 3).1 membrane electrochemical gradients and depletion of ATP reserves.15

Citation: Mendoza MCV, Martínez DDB. Multimodal cerebral perfusion monitoring, use at the patient’s bedside. Hos Pal Med Int Jnl. 2024;7(4):136‒141.
DOI: 10.15406/hpmij.2024.07.00258
 Copyright:
Multimodal cerebral perfusion monitoring, use at the patient’s bedside ©2024 Mendoza et al. 139

Neuroprotective strategies - Transcranial Doppler: allows us to measure blood velocities at the

level of cerebral blood vessels (peak systolic, peak diastolic and mean
When talking about neuroprotective strategies, it is important to cerebral blood velocities; as well as cerebral vascular resistances
be clear that there are some counter-regulatory mechanisms against reflected as the pulsatility index), these are a surrogate of cerebral
brain injury, which will become the goals to be met during our clinical blood flow either local or regional.17 Among the different data that we
assessment:12 can subtract from the Transcranial Doppler are:
- Core temperature below 37.5 in order to decrease disproportionate ● Increased velocities: vasospasm, stenosis. Anemia, hyperemia,
oxygen consumption. hyperthermia, hypervolemia, arterial hypertension, hypercapnia,
- Serum sodium between 135-145, maintaining this electrolyte in hypoxemia, volatile anesthetics.
normal ranges guarantees the adequate use of mitochondrial and ● Decreased velocities: age, hyperviscosity, dehydration, low
neuronal energy, as well as the transmission of signals. cardiac output, arterial hypotension, hypothermia, sedatives and
- Hemoglobin between 7-10 g/dl to ensure adequate oxygen hypnotics.
transport, however, this has a limitation, it does not assure us how ● Pulsatility index: Systolic velocity - Diastolic velocity/ Mean
well or poorly the hemoglobin protein is related to oxygen. velocity
- Serum glucose between 110 - 150 mg/dl, thus ensuring o Normal: 0.6 - 1.1
sufficient glucose for brain oxidation to provide energy for brain
requirements. o <0.6: vasospasm, hyperemia or high-grade stenosis.

- PaCo2 (partial pressure of carbon dioxide) between 35-40 o 1.2-1.6: intracranial hypertension or microangiopathy
mmHg which promotes neither deleterious vasodilatation nor o 1.7-3: severe hypertension
vasoconstriction in the patient with intracranial hypertension.
o >3: cerebral asystole
- Normal oxygenation parameters (oxygen saturation SaO2 >92%
and oxygen partial pressure PaO2 >90) which guarantee the 1. Optic nerve sheath diameter: approximation to indirect signs
necessary substrate to maintain minimal mitochondrial oxidation. of Endocranial hypertension by measuring the optic nerve sheath
diameter. This value is more representative in the acute moment.
- Normovolemia that will reflect less passage to the BBB and
less cerebral edema, in addition to the different hydroelectrolytic 0.5 cm = ICP > 20 mmHg
alterations.
2. Ptio2 catheter: local measurement of tissue oxygenation
Adhering to these strategies ensures that the minimal needs changes, positioned between the middle and anterior cerebral
necessary to maintain brain homeostasis are met. All this at the artery. It provides values that represent hypoxia levels.
bedside and recognizing that not all patients are equal responders.
-Poor prognosis is considered any period < 10mmHg during the
Neuro monitoring devices first 24h after brain injury or any period for more than 30 minutes.
Greater probability of death with levels ≤ 6 mmHg.
Currently there are several ways to monitor and follow up the
neuroprotective interventions carried out, being clear about what our - 15 mmHg: mild-moderate tissue hypoxia
goals are and what the information obtained from them will be useful - 10 mmHg: severe tissue hypoxia
for. Among the various diagnostic and therapeutic aids we have:12,14
- 5mmHg: critical tissue hypoxia.
- ICP/CPP measurement catheter: by means of this invasive device
we can determine the conduction pressure necessary to guarantee 3. NIRS device: it will provide information on cerebral oxygen
adequate cerebral perfusion, being relevant not only the value of this, delivery, measuring the absorption of oxygenated and non-
but also the morphology of the previously mentioned curve (Figure oxygenated hb to infrared light. Its normal values are 50-80%
4).13 in adults.18
4. Cerebral microdialysis: its main role is to know in a
microcirculatory way how the cerebral oxygen metabolism is,
being the method or device of choice for this type of question.
However, given the complications to measure it, it is less and
less used.
5. EEG: although it is one of the most complex and the most remote,
it provides information on CNS function from the electrical point
of view.
6. Sjvo2 catheter - Measurement of venous gases from the
Figure 4 ICP waves recorded at 25 mm/sec. showing its 3 components (P1, jugular gulf: allows us to evaluate the relationship between
P2, P3).13 cerebral blood flow and cerebral metabolic requirements. With
A, Wave with normal morphology; B, Predominant P2 pattern [Reduced these gases we can perform different calculations described in
Compliance]; C, Waves of image A and B in patient with Endocranial Table 3 & 4 and thus determine whether anaerobic metabolism
Hypertension. prevails in the brain, in order to subsequently establish what type
of hypoxia is related to the patient’s clinical condition.19

Citation: Mendoza MCV, Martínez DDB. Multimodal cerebral perfusion monitoring, use at the patient’s bedside. Hos Pal Med Int Jnl. 2024;7(4):136‒141.
DOI: 10.15406/hpmij.2024.07.00258
 Copyright:
Multimodal cerebral perfusion monitoring, use at the patient’s bedside ©2024 Mendoza et al. 140

Table 3 Brain metabolism formulas16

CaO2 = (1.34 × Hb × SaO2) +

Arterial oxygen content [CaO2] 17-20 ml/dl
(0.003 × paO2)
CvO2 = (1.34 × Hb × SjvO2) +
Venous oxygen content [CvO2] 12-15ml/dl
(0.003 × pjvO2)
[D(a-v)O2] <4 ml O2/100mL greater intake than consumption (flow
perfusion): hyperemia. FSC in excess in relation to requirements, decreased
Arterio-venous O2 difference
D(a-v)O2= CaO2 - CvO2 oxygen extraction. [D(a-v)O2] >8 ml O2/100mL consumption greater than
[D(a-v)O2]
input (ischemia): Hypoperfusion. FSC decreases in relation to requirements.
Increased oxygen extraction
Oxygen Extraction Cup [OER] OER = (CaO2 - CvO2)/CaO2 25-35%
Arteriovenous glucose AJVD glc = arterial glc - jugular-
0.2 - 0.8 mmol
difference [AJVD glc] venous glc
Lactate arteriovenous difference AJVD lac = arterial lac - jugular-
-0.2 - 0.2 mmol
[AJVD lact] venous lac
Oxygen Glucose Index [OGI] OGI = avDO2/AJVD glc >6 aerobic metabolism, lactate <6 anaerobic metabolism
lactate-glucose index [LGI] LGI = AJVD lact/AJVD glc LGI negative = lactate production; LGI positive = lactate uptake
LOI negative: lactate release (anaerobic) LOI Positive: lactate consumption
Lactate Oxygen Index [LOI] LOI = AJVD lact/ avDO2
(aerobiosis) Normal <0.03 >0.08 increase in lactate production = ischemia
Delta CO2 AJVD pCO2 = paCO2 - pjvCO2 Normal 6, >9 anaerobic metabolism
[AJVD pCO2] [AJVD pCO2
Hb, hemoglobin; SaO2, Arterial oxygen saturation; paO2, arterial oxygen pressure; SjvO2, venous oxygen saturation; pjvO2, venous oxygen pressure
Table 4 Interpretation of jugular gulf venous gas values18

SvyO2 value - interpretation

90 - 100% Very low metabolic activity, compatible with brain death, deep hypothermia or AVM
75 - 90% Absolute or relative hyperemia, compatible with late head trauma, hypercapnia or MAC
60 - 75% Normal value, does not exclude focal ischemia or infarction
50 - 60% Increased O2 extraction, compatible with no ischemia or mild ischemia
45 - 50% Moderate ischemia, should be associated with lactate determination
< 45% Severe ischemia, compatible with anaerobic metabolism. Urgent treatment is needed

Approach to the types of tissue hypoxia sufficient quantities, but do not use it. It is a state in which oxidative
energy production and glycolytic energy production are insufficient,
Tissue hypoxia is a state in which the cell and tissue do not receive leading to lactic acidosis and cellular malfunction. Eight causes of
sufficient oxygen supply according to their needs or receive it in tissue hypoxia have been described (Table 5).20–23
Table 5 Types of tissue hypoxia -CMRO2 cerebral metabolic oxygen consumption Multimodal cerebral perfusion monitoring, use at the patient’s bedside21

Hypoxia class PET profile Neuromonitoria profile

Ischemic FSC decrease Decrease CMRO2 Increase OEF PTiO2 low Increased lactate/pyruvate ratio
Disperfusion Normal FSC Normal OEF Decrease CMRO2 Normal PTiO2 Increased lactate/pyruvate ratio
Uncoupling Normal FSC Decrease OEF Decrease CMRO2 Normal PTiO2 Increased lactate/pyruvate ratio
Shunt Increase FSC Decrease/normal OEF Decreased/normal CMRO2 PTiO2 Normal Increased lactate/pyruvate ratio
Low extraction
● Hypoxic
Increased/ Normal FSC Increase/ Normal OEF Decrease CMRO2 PTiO2 low Increased lactate/pyruvate ratio
● Anemic
● High Affinity
Hypermetabolic Increase FSC Increase OEF Normal CMRO2 PTiO2 low Increased lactate/pyruvate ratio

Ischemic hypoxia: It occurs when there is insufficient cerebral blood Extraction hypoxia: conditions that generate a low extraction tension
flow, which will be determined by cerebral perfusion pressure, so a are grouped together. The extraction tension is understood as the
decrease in this, as well as a vasoconstriction or obstruction of flow can oxygen tension obtained after the extraction of a standard amount
cause. A decreased cardiac output will trigger systemic hypotension, it of oxygen per liter of blood. It indicates the degree of compensation
can also be secondary to peripheral vasodilatation. between arterial oxygen pressure, effective hemoglobin concentration
and mean saturation tension. Within this group are described:
Therapy: depends on the mechanism responsible for the reduction
in FSC. One can optimize MAT with fluids or vasopressor/inotropic Hypoxemic hypoxia due to low arterial pO2, abnormal oxygen
drugs, reduce ICP, correct hyperventilation, and treat vasospasm or exchange. It is associated with ventilation-perfusion mistmatch,
vessel occlusion with endovascular therapy. atelectasis, pulmonary contusion, pneumonia, mechanical ventilation
associated injury, ARDS.

Citation: Mendoza MCV, Martínez DDB. Multimodal cerebral perfusion monitoring, use at the patient’s bedside. Hos Pal Med Int Jnl. 2024;7(4):136‒141.
DOI: 10.15406/hpmij.2024.07.00258
 Copyright:
Multimodal cerebral perfusion monitoring, use at the patient’s bedside ©2024 Mendoza et al. 141

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Citation: Mendoza MCV, Martínez DDB. Multimodal cerebral perfusion monitoring, use at the patient’s bedside. Hos Pal Med Int Jnl. 2024;7(4):136‒141.
DOI: 10.15406/hpmij.2024.07.00258