protocols for brain oxygenation & cognitive recovery
TRANSCRIPT
ACIM OCTOBER 2015 ~ ORLANDO
TOM BUTLER, MSOM MARK SQUIBB, CEO
DR. ANGELIQUE HART, MD
Protocols for Brain Oxygenation & Cognitive Recovery
Tom Butler, MSOM
perspective Current events might indicate society is largely approaching Healthcare backwards
Equivalent to talking about how pedestrians keep getting in the way of automobiles
Suggest that health-creation is approached from a perspective that gives the right of way to the pedestrians
Taking a whole body approach to most health issues, especially, brain health, can revolutionize health practice, medicine and research
Good science is also helpful.
omst via Dr. von Ardenne
positive feedback loop
reversible switching
prioritized oxygen usage across the organ systems
dissolved oxygen in plasma to 4x normal is where the therapeutic benefits live
specialized roles
vessels of the same caliber in different organs are as different as the organ parenchymal cells through which they course
micro vascular bed components and the tissues they perfuse are designed to meet the special needs of different organs and even unique neighborhoods within organs
basic dis-function (1)Blood Micro Circulation
NEED Diagram Page 7 OMST book
The Endothelial Cell ( micro switch )
Reduced blood flow (< pO2 -ven reduced )
Increased viscosity ( patterns of blood stasis and stagnation )
H20 flows into the cells as a result of K+/Na+ pump (inflammation / edema of tissues )
Organ PrioritizationDiagram page 12 OMST book
blood
blood patterns
stasis
stagnation
blood cracking
loss of glutathione with age
protein degradation
oxygen delivery
three modes Red Blood Cells ( RBC ~ 98%)Plasma RBC water
Oxygen has a low solubility (CO competes)
Hemoglobin ~ 200 different structures
Primary Hemoglobin A
Variants have different O2 binding properties
shift to the left (hemoglobin)
dissolved fraction (plasma)
priority classes pO2-ven resting (mmHg) normal 30 yrs
Heart ~22Lower Ext ~ 28Brain ~ 33Upper Ext ~ 35Liver ~ 40Stomach/GI ~ 48Skin ~ 50 Kidney ~ 62Spleen ~ 68
What will override auto-regulation and trigger vasodilation?
bioenergy production
aerobic respiration “with air”Glucose + Oxygen > Carbon dioxide + Water + Energy
C6H12O6 + 6O2 > 6CO2 + 6H2O + 2900 kJ/mol
creates ~ 38-34 atp molecules / glucose
only net positive energy production availabe in body
anaerobic respiration “without air” Glucose > Lactic acid + Energy
C6H12O6 > 2C3H6O3 + 120 kJ/mol
creates ~ 2 atp molecules / glucose
not net positive ( lactic acid conversion -6 atp )
How is gene activation related to bioenergy?
bioenergy cascade
protein folding consumes 2/3 of cellular ATP by ER
protein quality control failure
degradation of blood brain barrier
unfolded protein response overwhelm
accumulation & aggregation of mis-folded proteins is the hallmark of most neurodegenerative diseases
mircobiota
Of 254 reference genomes, only 29 genomes (11%) are aerophilic, 111 (44%) are microaerophilic, and 115 (45%) are anaerobic.
symbiotic aerobic ( 55 % )
pathogenic anaerobic ( 45 % )
The details of the annotated respiratory reductases are captured as a subsystem “Respiration HGM”.
the basic protocol
whole body oxygenation
basic liveO2 protocol
~increased dissolved oxygen in plasma
~left shift affinity for hemoglobin binding to oxygen
~increase partial pressure
functionality
support of the whole is the basis of supporting
Neuroregeneration.
foundations
oxygenation
fluid balance
nutrition
Mark Squibb, CEO
cerebral hemodynamics
the brain uses 20% of available oxygen for normal function1
Radius is the most powerful determinant of coordinated blood flow2
keys to breakthrough auto regulation
cardiac output 3
altitude ( O2-)
Co2
NO
arterial blood pressure 4
systemic circuit flow
cbf normalThe human brain represents approximately 2% of total body weight, yet it receives approximately 20% of cardiac output and uses 20% of total body oxygen consumed under normal conditions. In this situation, most of the energy of the brain is obtained exclusively from aerobic metabolic process.
Impairment in the supply of nutrients and oxygen to the brain can cause cellular damage.
CBF varies directly with cerebral perfusion pressure (CPP), which is defined as the difference between mean arterial and intracranial pressures, and inversely with cerebrovascular resistance (the sum of vascular resistance to flow, particularly at the level of the small pial arteries and penetrating pre-capillary arterioles). The contribution of any given cerebral vessel to overall CBF is defined by factors, such as its radius and length, and both blood viscosity and pressure.
cbf regulationCerebral or pressure auto-regulation is the inherent ability of blood vessels to keep CBF relatively constant over a wide range of arterial blood pressure (ABP) levels by the interplay of numerous physiological mechanisms.
A sudden change in mean ABP leads to a simultaneous change in CBF initially, but it also triggers a number of other responses. For instance, ABP augmentation produces dilatation of cerebral arteries, which leads to a chain of events: changes in smooth muscle ionic permeability, muscle contraction, vessel narrowing, and increase in cerebrovascular resistance (myogenic mechanism).
Concomitantly, CBF elevation due to ABP augmentation causes both increase in tissue O2 and decrease in the concentration of CO2 and other products of cerebral metabolism. In the absence of greater demand for O2, a complex sequence of events restores the balance between O2 supply and demand by means of vasoconstriction mediated by activation of nitric oxide (NO) and other metabolites in the arterial endothelium (metabolic mechanism).
Recently, sympathetic neural control has been implicated as one of the mechanisms of cerebral auto-regulation (neurogenic mechanism)1.
CBF and ABP with increasing PE
cardiac output
There is a linear relationship between CBF velocity and cardiac output at rest and during exercise1.
Interestingly, decreased CBF velocity was confirmed even though mean arterial pressure was increased. This is possible due to the fact that the lowering of cardiac output can be accompanied by increases in arterial pressure. Therefore, in clinical practice, blood pressure augmentation may not necessarily imply an associated increase in CBF2.
The dependence of CBF on cardiac output is also seen in cardiac patients, in which decreased cerebral oxygenation during exercise can be noted in cardiac patients with decreased perfusion as a result of compromised cardiac output3.
high altitudeThe mechanisms underlying the regulation of CBF during acute exposure to high altitude are complex and depend partly on the degree of hypoxic stimulus and on the cerebrovascular sensitivity to hypoxia and CO2
1.
Neurological disorders associated with altitude have an intimate relationship with disturbances of cerebrovascular regulation due to high altitude and with the process of acclimatization. Subjects exposed to hypoxia at high altitudes develop an increase in steady-state CBF velocity associated with impairment of cerebral autoregulation2.
Note: patients with intracranial hematomas or some degree of brain swelling, irrespective of etiology, can develop or experience worsening intracranial hypertension when adapting through acute hypoxic events3.
inflammation
in the brain creates cellular noise that interferes with information processing
excitatory chemicals created by glial cells
neglected house keeping
irritation of excitotoxicity reinforces pattern
tuning
a brain with cell health problems will get detuned very easily
healthy brain has the best chance of being optimally tuned electrically
worse brain cell health: more noise + static + less signal = poor bandwidth
Can an adaptive response break or shift the pathology?
balance
the brain can be physically displaced by trauma
even subtle displacement can interfere with fluid circulation and nerve supply, and subtle brain movements associated with health
network synchronization
when different parts of the brain oscillate together at the same frequencies, this gets information transferred
synchronization is not just a function of hardware (like neuronal cables) but also of waves that move rapidly across the brain
Are adaptation events capable of resetting normal Oscillatory patterns and Synchronization of the Neural-networks?
premises
The brain has a high metabolic demand for oxygen. Acute hypoxia triggers dilation of cerebral microcirculation and increase in CBF
In general, CBF does not change substantially until tissue PO2 falls below 50 mmHg1. As hypoxia decreases PO2 further, CBF can rise to 400% of resting levels2.
Acute hypoxia can cause an increase in the CBF by means of direct effects on cerebral arterioles.
A hypoxia-induced decrease in ATP levels opens KATP channels in arteriole smooth muscle inducing hyperpolarization and vasodilation. Moreover, hypoxia rapidly increases NO and adenosine production resulting in vasodilation3
cognitive case 1 Patient History
Physiological systems model Condition(s) & Symptoms Quality of Life Improvement Initial versus final Speed of change Opinion of durability & maintenance Role of LiveO2 in change Generalization Clinical Results Blood Tests Other before/after testing
Protocol Body Systems targeted by protocol Protocol element list Reason for each Relationships Roles of LiveO2 – reasons Anti- Inflammatory? Hypoxic region? Immunological? Low energy tissues? Detox catalyst?
Efficacy Model Animated view of effect of therapy combination Affected tissues Energetic dysfunction Immune, etc. How LiveO2 oxygen catalyzes recovery Inflammatory inhibitor Regional hypoxia inhibitor
Doctor: What went wrong Did oxygen-deficiency in enable pathology Was there a stress event? Was there a probable systems failure process? Will avoidance of hypoxia improve prognosis? Usage Recommendation for Patient Daily, etc. Intensity
Why/how does doctor feel Live O2 will help this patient in the future Optimize Doctors opinion on quality of life with vs without Live 02
cognitive case 2 Patient History
Physiological systems model Condition(s) & Symptoms Quality of Life Improvement Initial versus final Speed of change Opinion of durability & maintenance Role of LiveO2 in change Generalization Clinical Results Blood Tests Other before/after testing
Protocol Body Systems targeted by protocol Protocol element list Reason for each Relationships Roles of LiveO2 – reasons Anti- Inflammatory? Hypoxic region? Immunological? Low energy tissues? Detox catalyst?
Efficacy Model Animated view of effect of therapy combination Affected tissues Energetic dysfunction Immune, etc. How LiveO2 oxygen catalyzes recovery Inflammatory inhibitor Regional hypoxia inhibitor
Doctor: What went wrong Did oxygen-deficiency in enable pathology Was there a stress event? Was there a probable systems failure process? Will avoidance of hypoxia improve prognosis? Usage Recommendation for Patient Daily, etc. Intensity
Why/how does doctor feel Live O2 will help this patient in the future Optimize Doctors opinion on quality of life with vs without Live 02
adaptive protocol
adaptive training keys
artifacts of being in the zone
Angelique Hart, MD
Case Study A Patient History Physiological systems model Condition(s) & Symptoms Quality of Life Improvement Initial versus final Speed of change Opinion of durability & maintenance Role of LiveO2 in change Generalization Clinical Results Blood Tests Other before/after testing
Protocol Body Systems targeted by protocol Protocol element list Reason for each Relationships Roles of LiveO2 – reasons Anti- Inflammatory? Hypoxic region? Immunological? Low energy tissues? Detox catalyst?
Efficacy Model Animated view of effect of therapy combination Affected tissues Energetic dysfunction Immune, etc. How LiveO2 oxygen catalyzes recovery Inflammatory inhibitor Regional hypoxia inhibitor
Doctor: What went wrong Did oxygen-deficiency in enable pathology Was there a stress event? Was there a probable systems failure process? Will avoidance of hypoxia improve prognosis? Usage Recommendation for Patient Daily, etc. Intensity
Why/how does doctor feel Live O2 will help this patient in the future Optimize Doctors opinion on quality of life with vs without Live 02
Case Study B Patient History Physiological systems model Condition(s) & Symptoms Quality of Life Improvement Initial versus final Speed of change Opinion of durability & maintenance Role of LiveO2 in change Generalization Clinical Results Blood Tests Other before/after testing
Protocol Body Systems targeted by protocol Protocol element list Reason for each Relationships Roles of LiveO2 – reasons Anti- Inflammatory? Hypoxic region? Immunological? Low energy tissues? Detox catalyst?
Efficacy Model Animated view of effect of therapy combination Affected tissues Energetic dysfunction Immune, etc. How LiveO2 oxygen catalyzes recovery Inflammatory inhibitor Regional hypoxia inhibitor
Doctor: What went wrong Did oxygen-deficiency in enable pathology Was there a stress event? Was there a probable systems failure process? Will avoidance of hypoxia improve prognosis? Usage Recommendation for Patient Daily, etc. Intensity
Why/how does doctor feel Live O2 will help this patient in the future Optimize Doctors opinion on quality of life with vs without Live 02
clinical protocols
#1takeaway
”obstruction of capacities rather than impairment”
re-balance
questions
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