Aetiology and Pathogenesis
of Acute High Altitude Sickness
Analysis from the new scientific
perspective of the Lung as a mechanically active autonomic organ, under Vagus
Sympathetic complementary command
Abstract
Low air mass per volume unit at high altitude
is the cause of acute mountain sickness.
The autonomic cyclic
mechanics of the Lung start by contraction
of the muscles of the lobar bronchi and those of the lobular bronchioles,
which while decreasing their capacities, proportionally increase the molecular
mass per volume unit of the inspired air, thus increasing their molecular
expansive forces.
These dynamics lead
to displacement of the contained air in the sense towards lower resistance,
to then expand the pulmonary structures in balanced forces, once muscular
relaxation begins. Finally, the tiny intra-alveolar air masses distend
the alveolar wall in balance with capillary blood pressure.
These processes are
accomplished by two kinds of dynamic cycles
1.
Lobar cycles, for air renovation, under Vagus Nerve command.
2.
Lobular cycles, for gas exchange with the blood, under Sympathetic Nerve
command.
If the atmospheric
mass of air per volume unit were lower to that demanded by the adaptation
limits of the human specie, its molecular expansive force would be insufficient
to achieve pulmonary dynamic expansion, with all that implies, as described
above.
Therefore, the
expansive molecular forces of the alveolar air mass would be insufficient
to expand the alveoli with the required tension to enable the right balance
of blood and air pressure for balance for selective diffusion of Oxygen. The
consequence would be pulmonary arterial blood hypertension, hypoxemia and
pulmonary oedema, as is the case in Acute Mountain Sickness.
Simultaneous data
and graphs of Resultants of these dynamics, discovered by the Author in 1978,
in the pleural space of experimental dogs, are analyzed. Related Author’s
published works are: “Fisiodinámica del Hombre en el Mundo” "The New
Theory of Respiratory Dynamics" "Integración Dinámico Funcional del Organismo Viviente". The Aetiology and
Pathogenesis of Acute Mountain Sickness
Purpose
This work, carried out during the year 2000, obeys to my aim of applying the scientific basis of the Pulmonary autonomic mechanics, developed by me during more than twenty two years, to understand the Acute Mechanical failure of the Lung dynamics at High Altitude, known as Acute High Altitude Sickness, with the hope of contributing with its prevention and effective speedy treatment avoiding complications
Introductory Remarks
Rigorous
interpretation of this Discovery, which represents a historical landmark,
led me to define two different kinds of cyclic activity: One that comprises
the whole cycle, coincident with the breathing cycles and the other, a series
of minor cycles coincident with cardiac cycles, both clinically determined
This complex Resultant is generated by cyclic variation of forces transmitted to the pulmonary surface, which origin and development merit to be analysed.
Hence, applying the Newton’s Inertial Principle F = m .a (force equals mass per acceleration) it is compulsory to determine the source of the forces, the identity of the mass, and the space limiting its acceleration, as well as the causes of the periods of those cyclic displacements
The Force
The main working forces concurrent to the performance of the Respiratory Cycles have two complementary sources, leading to complementary objectives:
Sources of the forces
1.
Universal
Dynamics, mediated by the Atmosphere of the Earth
2.
The Living
Organism
We can identify, by abstraction, the origin of some partial forces and their objectives
1.Atmospheric
force’s origin, relative to altitude
Altitude means distance from
sea level, in essence, distance from the centre of the Earth, from which its
gravitational force is exerted. This force, applied on the Atmosphere, determines
its length, relative to the weight of its column of air, the value of which
at sea level is 76 cm Hg.
In other words: the mass
of a column of atmospheric air at sea level is 76 cm Hg and, from it, approximately
21% corresponds to Oxygen, with a partial pressure of about 15,96 cm Hg. And
79% corresponds to Nitrogen, with a partial pressure of 60,4 cm Hg.
Now, this pressure corresponds
to the lower level of human adaptation in our natural habitat. If the
pressure is increased for any cause, it will be increased the Resultant force
needed for the diffusion of gases, firstly Oxygen, surpassing the capacity
of fixation by the haemoglobin of the blood and the dissolved Oxygen will
increase.
If distension of the alveolar
structure increases farther on, Nitrogen would also diffuse, with the danger
of gaseous emboli
The mass of atmospheric air and with its proportional masses of Oxygen and Nitrogen decrease during ascent from sea level, because the air column at each upper level diminishes. One most add to this, temperature and humidity, among other factors, with the consequences above mentioned. These elemental concepts need no discussion.
2. Organic
forces’s Origin
1.
Contraction-relaxation of the airways smooth muscles
2.
Expansive molecular force of the gasses pressurised in each
sector of the bronchial and bronchiolar trees
3.
Capillary blood heat transfer to the alveolar air mass
4.
Reflex contraction-relaxation of the Diaphragmatic Belt
of striated muscles
5.
Contraction-relaxation of the right ventricle
The pulmonary bronchial
and bronchiolar structures are well known, as also are their muscular fibres
distribution as geodesic networks and sphincters, whose contraction
generates the necessary energy to decrease the diameters and length of those
passages, with three main consequent effects
1.
Proportional reduction in their capacities
2.
Simultaneous proportional widening of the pleural
lumen,
3.
Momentarily closure of the airways, by segments.
Physiological objectives of the lobar bronchi
muscular contraction
1. To increase pressure in the lobar bronchi contained air, in accordance with the Boyle Mariotte Principle V.P = C (Volume per Pressure is a Constant.). This pressure increase means accumulation of potential energy, as expansive molecular forces
2. To generate Pulmo-diaphragmatic (Vago-Phrenic) mechanical reflex to incorporate the working effects of the Diaphragmatic Belt. That is to say, to evoke Diaphragm contraction, followed by automatic somato-somatic reflexes (Diaphragm-intercostals and abdominal muscles) (2)
3. To increase the pleural lumen, in order to decrease resistance to pulmonary gases expansion and arterial blood circulation
Physiological objectives of the lobar bronchi
muscular relaxation
1. Displacement of the previously pressurised gases towards their destination on the pulmonary periphery, by own molecular expansion, expanding the Lung, to accomplish immediate and mediate ends
2. Decrease resistance for intrapulmonary gas expansion, with abdominal press effect towards the low abdomen
3. Abdominal muscles contraction (Diaphragmatic Belt), with press effect towards the thorax
4. Intercostal muscles contraction for thorax expansion (Diaphragmatic Belt), with floodgate effect, decreasing resistance to abdominal blood stream towards the Thorax
The mass.
The intrapulmonary working factor mass is the mass of air contained in each sector of the air passages, bronchial and bronchiolar, directly renovated from the right and left main bronchi and the Trachea, where the air formerly inspired is pre-acclimatised, that is to say, the mass per volume unit of the atmospheric air is pre-adapted, along the extra pulmonary airways, to physical conditions physiologically demanded, between limits genetically programmed for use and final adaptation in the intra-pulmonary airways, while also accomplishes simultaneous, successive and integrated physiological dynamic effects, for a final pulmonary result at the alveolar level, enabling eupnoea
Acceleration: e/t (space divided by time)
The space is anatomically defined by the length of one file of bronchi and bronchioles up to their alveoli, while the time is physiologically determined by the period of the concerned cycles, which change in relation with organic demands, under control of the Vagus and Sympathetic nerves
Physiological Objectives of the Lobular Bronchiole’s
Muscles contraction
Dynamics of the lobular bronchioles is similar, in general sense, to the dynamics of the lobar bronchi, with differences relative to the magnitude of factors as well as local effects and objectives
To understand the Aetiology
and pathogenesis of AHAS it is necessary to know the normal dynamics of the
Lung in the habitat of natural adaptation of the species, as synthesised in
the introductory Remarks
Living species and individuals
are mechanical structures genetically designed for dynamical integration with
the Atmosphere, at the very moment of birth, and adaptation to different levels
of altitude, within their own limits, relative to the mass of air per
volume unit.
It is well known that the respiratory function of healthy individuals, in their local habitat, disposes of a wide adaptation range to organic demands, relative to physical activity
A wider concept of Habitat is Natural Habitat of Species and Individuals Adaptation, which is genetically determined and infers the concept of Altitude above sea level, this relative to the distance from the centre of the Earth, as determinant of its Gravitation Force and, with it, atmospheric pressure at different geographical levels, which is relative to the mass of air per volume unit
We are now starting focussing the Aetiology of Acute High Altitude Sickness, which is relative to the functional binomial Man-Earth of which the factor Man is the same and, only one element of the factor Earth has changed: the distance from sea level and its consequent effect on the mass per volume unit of atmospheric air, which I pointed out as the Cause of the sickness.
Low air mass per volume unit above the upper
limit of human natural adaptation is the cause of the acute failure of the
Lung dynamics known as Acute High Altitude Sickness
Pathogenesis
Acute High Altitude Sickness
is well known as the sum of signs and symptoms observed in otherwise normal
individuals when displaced at high altitude. Therefore, one needs to know
how does the binomial Man-mass of air at sea level works, for gas exchange
with the blood
The Physical factor Man
is represented in this moment of my analysis by the joint of the lobular
units of each and all the lobes in their ensemble, since the lobules receive
the masses of air previously adapted along the airways and are the dynamic-functional
units for development of the specific cycle leading to gas exchange with the
blood, while the alveoli are surface units for Oxygen diffusion, under
effect of the expansive molecular forces of the tiny masses of gases displaced
up to them.
Mechanical Actions and Effects
1. Lobular Floodgate actions and effects in the pleural space
Retraction of the lobular structure, as a consequence of its bronchioles muscular contraction, widens the pleural lumen to decrease resistance to pulmonary arteriolar blood circulation towards the alveolar capillaries. Floodgate action and effect

Fig
1. Simultaneous graphs of three main parameters from top to bottoms: 1. Respiratory
Pulse: 2. Intra-pleural sub-atmospheric pressure Abdominal aortic pulses The
circles defines each lobular alveolo-capillary cycle and the correspondences
with the others parameters. The arrows mark the coincident inflexion of capillary
and arterial pulses (Graph taken from my book “The New Theory of Respiratory
Dynamics”) (2)
2. Lobular Press action by molecular expansion of the air mass displaced up
to the alveoli, distend the alveolo-capillary
membrane, leading to two simultaneous effects:
2.1
Oxygen selective diffusion
2.2
Press effect to displace the oxygenated blood towards the pulmonary veins
Therefore, decrease in alveolar membrane distension generates two well-known signs characterising the beginning of this sickness
1. Hypoxemia because insufficient distension of the alveolar membrane, distorting Oxygen diffusion
2. Pulmonary arterial hypertension, because low alveolar-capillary press action, causing partial retention of pulmonary arteriolar circulation
On the basis of the above
general explanation, I consider it useful to discuss now important clinical
and anatomopathologic observations carried out by different authors under
various conditions and/or stages of this sickness, but whose interpretations,
based on the traditional theory that considers the Lung a passive organ, has
been unable to define neither the cause nor the pathogenesis not even the
precise rational prevention and treatment, all of which constitutes the purpose
of this work.
Hurtado first demonstrated
that pulmonary arterial hypertension in humans; this is a sign in patients
with this sickness (6)
Hurtado et all observe that
Oxygen partially prevents the rise in pulmonary arterial pressure in exercise.
Arias Stella et all (7), found
that excessive muscularisation of distal muscular arteries and arterioles
is a prominent feature of the pulmonary arterial bed of native highlanders.
Pulmonary hypertension
and hypoxia are the two most characteristic signs of the Acute High Altitude
Sickness because they are the two immediate consequences of the mechanical
unbalance generated at the alveolar-capillary level, by means of the two mechanical
effects described above:
2.1 Oxygen diffusion, causing hypoxia and
2.2 Displacement of the Oxygenated blood causing retrograde
retention of the pulmonary arterial blood, with hypertension
The observation
that acute administration of Oxygen caused little or no fall in pulmonary
vascular resistance at rest and that Oxygen partially prevents the rise in
pulmonary arterial pressure in exercise (6) are also consistent with our mechanical
interpretation since the problem is not lack of Oxygen or hypoxia but lack
of enough total air mass. If acute administration of Oxygen prevents rise
in pulmonary arterial pressure is because the patient was partially-adapted
to that altitude and the additional Oxygen supply the extra-demand because
exercise, as in any patient suffering from respiratory insufficiency
The excessive muscularisation
of the named arterial vessels is an expected anatomopathological consequence,
because excessive repeated muscular contraction to overcome the functional
obstruction due to lack of alveolar capillary press action and effect
Peñaloza, Arias Stella et
all (8), observe that pulmonary arterial pressure during childhood is higher
at altitude than at sea level.
This observation obeys to
the same mechanical cause as exposed above
Grover et all (9) and Sime
et all (10) state that “prolonged removal of the hypoxic stimulus by descent
to sea level result in the fall of pulmonary arterial pressure and pulmonary
vascular resistance to normal values for lowlanders.
The observations
are correct, but the interpretation is wrong. The correct interpretation must
be: descent to sea level result in the fall of pulmonary arterial hypertension
and pulmonary resistance to the arterial flow because the lung dynamics has
recuperated after restitution of a mass of air per volume unit between the
limits of natural adaptation.
Reaves and Grover (11) observe
that in newborns breathing ambient air, the fall in pulmonary arterial pressure
during the first three days of life is less marked than at sea level and Peñalosa
et all (12). Arias-Stella et all (13) observe that throughout childhood pulmonary
arterial pressure is higher at altitude than at sea level.
Important observations. Their interpretations are similar to those
explained above.
Kronenberg et all (14), observe
that arterial pressure in individuals coming from low lands increased after
a few minutes of exposure to altitudes, reaching a plateau after 12 to 24
hours, being reversible by Oxygen administration.
This observations
are of theoretical and practical importance since they refers to a relative
period in which the strength for adaptation is near its limit and Oxygen administration
supply a little amount of the factor mass
Hurtado and others (15, 16)
found that systolic peripheral blood pressure was lower in practically all
subjects studied.
This very important observation
is compatible with re-distribution of the blood because of failure of mechanical
factors developed by the thoracic-abdominal muscular and costal belt, as described
by me elsewhere.
In synthesis, all
these observations, as discussed here, are coherent with expectations derived
from my discoveries and their interpretations of pulmonary mechanics, pulmo-cardiac
dynamic integration, as well as with the integration and balance of our organisms
with the Atmosphere of the Earth
This pathology is
generally interpreted as caused by hypoxia, which is consequent with the prevailing
traditional theory of Respiration that considers the lung a mechanically passive
organ and, Oxygen, as the gas useful for respiration, since this is the gas
necessary for organic metabolism
Discussion.
The Living being,
is a complex integrated structural and functional organization, for
maintenance of created life in its natural habitat of adaptation, mainly relative
to altitude
To achieve this purpose disposes
of necessary parameters for balance of actions, reactions and functional integrations,
in the dynamic balance characterising Life and Health, made objective as eupnoea
(3)
Let us now to analyse the posed
problem, from the new scientific perspective of the Lung as a mechanically
autonomic active organ working under Vagus Sympathetic complementary command.
I discovered the
autonomic Resultant of cyclic pressure variations of the pulmonary mechanics,
in its pleural surface (Respiratory Pulse) then, I analysed and interpreted
its two main cyclic components:
One that embraces the whole
cycle knew as “Respiratory”, which is only relative to air renovation
from the Atmosphere, being generated by lobar bronchial mechanics under Vagus
control.
The other, riding on the first:
the lobular-alveolar-capillary pulses or respiratory pulses strictus
sense (pulses for gas exchange with the blood), which are synchronous with
the cardiac pulses. (2)
Forces for air impulsion
and auto-impulsion into the alveoli must balance the alveolar-capillary
blood pressure. The Sympathetic System coordinates this complex physiological
integration.
I have fully described elsewhere
the functional alveolar-capillary units, which represent the pulmo-
cardiac functional integration as a necessary condition. Consequently,
obeying Sympathetic Adrenergic control, on a vagal dynamic basis.
Let us now to discuss the following:
What
does the concept Altitude mean, from the scientific physic-mathematical
analysis and, how does this affect the physiology of living beings, humans
among them?
Altitude means distance from
sea level, in essence, distance from the centre of the Earth, from which its
gravitational force is exerted. This force, applied on the Atmosphere, determines
its length, relative to the weight of its column of air, the value of which
at sea level is 76 cm Hg.
In other words: the mass
of a column of atmospheric air at sea level is 76 cm Hg and, from it, approximately
21% corresponds to Oxygen, with a partial pressure of about 15,96 cm Hg. And
79% corresponds to Nitrogen, with a partial pressure of 60,4 cm Hg.
Now, this pressure corresponds
to the lower level of adaptation in our natural habitat. If the pressure
increases for any cause, it will increase the Resultant force needed for the
diffusion of gases, firstly Oxygen, surpassing the capacity of fixation by
the haemoglobin of the blood and the dissolved Oxygen will increase.
If distension of the alveolar
structure increases farther on, Nitrogen would also diffuse, with the danger
of gaseous emboli
On the contrary, the mass of total air and the proportional masses of Oxygen and Nitrogen decrease during ascent from sea level, since the air column diminishes. One most add to this, temperature and humidity, among other factors, with the consequences above mentioned. These elemental concepts need no discussion.
The Living being, as a complex
integrated structural and functional organization, for maintenance of
created life in its natural habitat of adaptation, disposes of necessary parameters
for balance of actions, reactions and functional integrations, in the dynamic
balance characterising Life and Health, objectified as eupnoea (3)
We
can pose the following questions
In the light of my discoveries,
analysis and interpretations, the prevailing theory of respiratory mechanics
does not give and can not give a single rigorous answer since cyclic transportation
of air masses obey pulmonary dynamic phenomena on one side and physiological
demands on the other.
I have fully demonstrated,
for over twenty-two years, not only that the Lung is an autonomous mechanically
active organ, but also I have interpreted this activity on a Physic mathematical
basis, for physiological application.
Any Volume of inspired
air, at any altitude has a correlative mass. Volume-mass that
must be displaced throughout the airways in conditions of pressure, humidity
and temperature physiologically determined, during a time relative to
the integrated simultaneous rhythms, generated by their autonomous innervations,
which also determine the contracting force of the airways muscular fibres,
generating proportional variations in their respective capacities and also
simultaneous closure, due to sphincters action (sphincterlike of Miller).
This mechanics is the essence
for air transportation, since according to Newton’s Inertial Law, I repeat,
any displaced mass is a result of a force applied on it, which exerts an acceleration
expressed by the equation F = m .
a, from which the equations m = F/a
and a = F/m. are deduced.
The space for displacement
of the air mass does not change, since this is the length of the named airways.
Consequently, the variables are:
Coordination of these dynamic
factors are necessary for simultaneous displacement of the variable masses
per volume unit, towards intermediate and final destinations, in required
physical (physiological) conditions; to enable selective diffusion of Oxygen
in the required amount, to satisfy the demand of load by the haemoglobin of
the red cells simultaneously circulating throughout the alveolar capillaries.
The previous paragraphs contain
the utmost factors of the problem and pose the need for an explanation about
the how’s and why’s of the variables and their conditions, with physic mathematical
perspectives.
The smooth muscular
networks of the airways, correlative to the local and integrated functional
tasks of bronchi and bronchioles, included the fibres disposed as sphincters,
on contracting in response to Vagal and Sympathetic nerves discharges, decrease
the capacities of their corresponding airways, also closing them momentarily.
Consequently, this muscular contraction proportionally pressurise the contained
air masses, increasing their mass per volume unit (Boyle-Mariotte Law) also
accumulating expansive potential forces to be used during the relaxation period.
When muscular relaxation
starts, the expansive force of the gas molecules of the air, previously pressurised,
displace themselves in the sense of lower resistance, that is to say towards
the destinations programmed in the organic design, immediate and mediate,
the alveoli being their final pulmonary destination
The mass of inspired air
is simultaneously displaced throughout the different sectors, bronchi, bronchioles,
during simultaneous and successive steps.
I have defined four periodical sectors: (4)
I shall avoid here the two
first sectors, explained apart, and will only refer to the third and fourth,
which are closely related to specific pulmonary structures and constitute
the first dynamic step of the posed problem.
Relaxation of the lobar
bronchial muscles generate a sucking force against the air masses supplied
by the right and left major bronchi.
Those masses of air shall fill the capacities left empty by the former displacement
of the air masses retained for acclimatisation during the former cycle. This
process is simultaneously followed by displacing the air now filling the upper
airways and finally the air from the Atmosphere. This latter is the only objective
act defining Inspiration in the traditional sense. (5)
The next muscular contraction,
due to the Vagus nerve discharge will decrease the bronchial capacity thus
pressurising the intra-bronchial mass of air. This fact is followed by muscles
relaxation, opening ways for the air mass displacement towards the pulmonary
periphery, in order to supply the quote of air demanded by each and all the
lobules.
Simultaneously, the same
muscular contraction, when retracts pulls from the parietal pleuras, widening the pleural lumen, creating potential space
for pulmonary gases expansion with to effects flood gate and press action
to balance fluids circulation
It is obvious that
if the mass per volume unit of the inspired air is inferior to that
required by the dynamics in progress, the effects produced by the actions
and reactions derived from the muscular-increased contracting force, will
become proportionally increased and, even with the maximal effort of compensation
facing the final balance, Oxygen diffusion will not suffice, and the anoxic
effect will occur. Besides, parallel mechanical effects generating signs
and symptoms characterising Mountain Sickness will also be produced, these
latter mechanical effects generally ignored until now.
It is clear that the anoxia
in the tissues is a consequence of the primary mechanical problem generated
by insufficient mass of inspired air.
I must emphasise the fact that the posed general
problem is Insufficient air “mass”, in relation to that required by
the pulmonary functional structure, which is designed to generate and develop
the mechanical process needed to achieve the functions enabling Life and Health
in the natural environment of adaptation of the species and individuals.
The air mass
per volume unit supplied at higher altitudes to that of the species adaptation
limits results insufficient to distend the pulmonary structures and further
along, the alveolar-capillary membranes, generating organic dynamic unbalance.
The functional insufficiency
becomes evident once the potential capacity of action of the pulmonary structure
is exhausted. It is necessary to insist that the maximal nervous discharges
enhance maximal muscular contractions, able to decrease the bronchial capacity
up to the limit allowed by the structure of cartilages, which guarantee the
permanent filling by “residual air” as a condition for homogeneous cyclic
air circulation
Let’s now think in another
simultaneously important problem. The pulmonary blood vessels are distributed
in parallel with the airways and, elastic and collagen fibres surround both
kinds of passages, making them co-participant in common mechanical phenomena
Prevention.
It is necessary
to know the maximal altitude of physiological adaptation of the Human Living
Being’s vital structures and, to make aware that if that limit is surpassed,
individuals must be provided with chambers or tents of total pressurised
air, relative to the adaptation level of the group or individual.
Administration of pure Oxygen
has been widely used in prevention and even in therapy, as result of the fact
that the autonomic pulmonary mechanics and its direct relationship with the
gaseous mass of air are still unknown. As a consequence, the results have
not often been satisfactory and, when they look like being, it would be interesting
to analyse the conditions of the individuals as well as all the conditions
implicit in the supplied measures
Living Beings in the environment
of their natural integration and adaptation, constitute an Organo-Physical
Natural-Unit genetically designed to accomplish basic dynamic functions
as an Autonomic Balanced Mechanical System of Fluids, for which the
inspired atmospheric mass of air per volume unit, at the human adaptation
limit is the physic-natural factor for integration and balance, when satisfying
the organic demand for its basic physiological performance, accomplishing
the equation of the Inertial principle F = m . a.
2. The Atmosphere of the Earth, between the
geographic limits of adaptation of the specie, which supplies the air mass
per volume unit that corresponds to the organic genetic design
Acute High Altitude Sickness is the joint
of signs and symptoms derived from organic dynamic insufficiency due to a
mass of air supply inferior to that required for the organic dynamic balance
The Living Being is a functional
structure designed to maintain the created life in its natural habitat
The natural habitat of the
humans is the surface of the Earth and its Atmosphere, between limits genetically
established
The Lung is the organ responsible
for this dynamic integration
The pulmonary lobules are
the structures to accomplish the final step of the necessary balance, at alveolar
capillary level
The two factors integrate
dynamically at the very moment of berth, direct and primarily by the pulmonary
functional structure, in its thoracic ensemble. The factor of integration
and balance of the pulmonary dynamics and Universal dynamics is the air mass
per volume unit, which is relative to the altitude also relative to the Earth
force of gravity
The tiny masses
of air distributed among the alveoli exert expansive forces to distend the
alveolo-capillary membranes, with two objectives.
1.
To widen the pores of diffusion
to open way to the Oxygen molecule and not to that of Nitrogen
2.
To simultaneously perform press
action to displace the oxygenated blood towards the pulmonary veins
Scarce air mass determines
compensatory increase in the bronchiolar muscles contraction up to the potential
limit, after which hypoxemia and pulmonary hypertension with alveolar infiltration
and oedema starts to manifest
If the problem persists, the organic dynamics
farther than the pulmonary limits, starts to manifest as pulmonary and cerebral
oedema
1.
González-Bogen A. "Fisiodinámica
del Hombre en el Mundo" 1979. Ediciones de la Biblioteca U.C.V. P.O.Box
47004. Caracas 1040, Venezuela.
2.
González-Bogen A. "The
New Theory of Respiratory Dynamics". 1985. Ediciones de la Biblioteca.
U.C.V.
3.
González-Bogen A.
"Integración Dinámico-funcional del Organismo-Viviente" 1989.Ediciones
de la Biblioteca. U.C.V.
4.
González-Bogen A. International
Seminar "The Respiratory Pulse" Scientific Review. 1992. Year 1.
Nº1. 1992. and Year 2. Nº2.
1993.
5.
Web site
http://www.the-respiratory-pulse.org.ve/
6.
Rotta, A., Cánepa, A., Hurtado, A.,Velazquez, T., & Chavez, T.
(1956) Pulmonary circulation at sea level and at high altitudes. Journal of
Applied Physiology, 9, 328-336.
7. Arias-Stella,
J. & Saldaña, M. (1963) The terminal portion of the pulmonary vascular
tree in people native to high altitudes. Circulation, 28, 915-925.
8. Peñaloza, D., Arias-Stella, F. Sime F., Recavarren,
S. & Marticorena E. (1964) The heart and pulmonary circulation in children
atn high altitudes. Pediatrics, 34, 568-582.
9. Grover, R.F., Hill, D.H., Reeves, J. T., Weir, E.K., McMurtry,
I.F., & Alexander, A.F. (1975) Pulmonary hypertension at altitude. Progress
in respiratory research, vol. 9 pp 112-117. Karger, Basel
10. Sime, F., Peñaloza, D. & Ruiz, L.(1971)
Bradicardia, increased cardiac output, and reversal of pulmonary hypertension
in altitude natives living at sea level. British Heart Journal, 33, 647-657.
11. Reeves, John T., Bertron M. Groves, John R.
Sutton, Peter D. Wagner, Allen Cymerman, Mark K. Malconian, Paul B. Rock,
Patricia M. Young, and Charles S.
12. Peñaloza, D., Sime, F., Banchero, N., Gamboa,
R., Cruz,J., and Marticorena, E.: Pulmonary hypertension in healthy men born
and living at high altitudes. Am.
J. Cardiol. 11: 150, 1963.
13. Arias-Stella, J., and
Kruger, H., Pathology of high altitude pulmonary oedema. Arch. Path. 76: 147, 1963
14. Kronenberg 1970
15. Hurtado,
A., Merino, C. and Delgado, E. Arch. Int. Med. 75: 284,1945.
16. Hurtado, A., T. Velazquez, C. Reynafarje, R. Lozano, R. Chavez,
H.Aste Salazar, B. Reynafarje, C. Sánchez and J. Muñoz. Report to the USAF School of Medicine,
1954.
Author: Américo González-Bogen.
E
mail agbogen@reacciun.ve/
Web
site: www.the-respiratory-pulse.org.ve
Institution:
Foundation The Respiratory Pulse
Address:
Av. Universitaria. Edif. Caribana 43. Valle Abajo. Caracas
1040. Venezuela.
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