Surgery – Respiratory method or device – Means for mixing treating agent with respiratory gas
Reexamination Certificate
1999-09-08
2002-03-12
Weiss, John G. (Department: 3761)
Surgery
Respiratory method or device
Means for mixing treating agent with respiratory gas
C128S204230, C128S205280
Reexamination Certificate
active
06354292
ABSTRACT:
FIELD OF INVENTION
The purpose of this invention is to provide a simple breathing circuit that can, for example, be added to a standard circle anaesthetic circuit known to persons skilled in the art to hasten recovery of patients administered vapour anaesthetics prior to an operation.
This invention also relates to the use of the breathing circuit in hastening the recovery of patients who have been administered vapour anaesthetics prior to a surgical operation.
This invention also relates to methods of treatment of patients to hasten their recovery from administration of the vapour anaesthetics to them prior to surgical procedures.
BACKGROUND OF THE INVENTION
Physiology
Venous blood returns to the heart from the muscles and organs depleted of oxygen (O
2
) and full of carbon dioxide (CO
2
). Blood from various parts of the body is mixed in the heart (mixed venous blood) and pumped to the lungs. In the lungs the blood vessels break up into a net of small vessels surrounding tiny lung sacs (alveoli). The net of vessels surrounding the alveoli provides a large surface area for the exchange of gases by diffusion along their concentration gradients. A concentration gradient exists between the partial pressure of CO
2
(PCO
2
) in the mixed venous blood (PvCO
2
) and the alveolar PCO
2
. The CO
2
diffuses into the alveoli from the mixed venous blood from the beginning of inspiration until an equilibrium is reached between the PvCO
2
and the alveolar PCO
2
at some time during the breath. When the subject exhales, the end of his exhalation is considered to have come from the alveoli and reflect the equilibrium concentration between the capillaries and the alveoli; the PCO
2
in this gas is called end-tidal PCO
2
(P
ET
CO
2
).
When the blood passes the alveoli and is pumped by the heart to the arteries it is known as the arterial PCO
2
(PaCO
2
). The arterial blood has a PCO
2
equal to the PCO
2
at equilibrium between the capillaries and alveoli. With each breath some CO
2
is eliminated and fresh air containing little CO
2
(assumed to be O) is inhaled and dilutes the residual alveolar PCO
2
, establishing a new gradient for CO
2
to diffuse out of the mixed venous blood into the alveoli. The rate of breathing, or ventilation (V), usually expressed in L/min, is exactly that required to eliminate the CO
2
brought to the lungs and maintain an equilibrium PCO
2
(and PaCO
2
) of approximately 40 mmHg (in normal humans). When one produces more CO
2
(e.g. as a result of fever or exercise), more CO
2
is produced and carried to the lungs. One then has to breathe harder (hyperventilate) to wash out the extra CO
2
from the alveoli, and thus maintain the same equilibrium PaCO
2
. But if the CO
2
production stays normal, and one hyperventilates, then the PaCO
2
falls.
It is important to note that not all V contributes to blowing off CO
2
. Some V goes to the air passages (trachea and bronchi) and alveoli with little blood perfusing them, and thus doesn't contribute to blowing off CO
2
. That portion of V that goes to well perfused alveoli and participates in gas exchange is called the alveolar ventilation (VA).
There are a number of circumstances in therapeutic medicine and research where we want the subject to breathe harder but not change his PaCO
2
(see Table 1).
TABLE 1
Method of
Type of Investigation
Reference
adjustment
Source of CO
2
Respiratory muscle fatigue
5
M
R
12
M
E
7
M
R
Respiratory muscle training
2
M
R
3
M
R
Increased V during
6
M
R
anaesthesia
Carotid chemoreceptor
8
M
E
function
1
M
E
Effect of hypoxia on
10
M
E
sympathetic response
4
M
E
Control of respiration
9
A
E
Tracheobronchial tone
11
M
E
Table 1:
Title: Summary of previous studies attempting to maintain constant P
ET
CO
2
during hyperpnea
Legend: Method of adjustment of inspired PCO
2
: M=manual; A=automated. Source of CO
2
: R=rebreathing; E=external.
1. Angell-James, J. E., Clarke, J. A., de Burgh Daly, M. and Taton, A., Carotid chemoreceptor function and structure in the atherosclerotic rabbit: respiratory and cardiovascular responses to hyperoxia and hypercapnia.
Cardiovascular Research
23(6): 541-53, 1989.
2. Belman, M. J. and C. Mittman. Ventilatory muscle training improves exercise capacity in chronic obstructive pulmonary disease patients.
Am. Rev. Respir. Dis
. 121:273-280, 1980.
3. Bradley, M. E. and Leith, D. E. Ventilatory muscle training and the oxygen cost of sustained hyperpnea.
J. Appl. Physiol
. 45(6):885-892, 1978.
4. Busija, D. W., Orr, J. A., Rankin, J. G. H., Liang, H. K. and Wagerle, L. C., Cerebral blood flow during normocapnic hyperoxia in the unanaesthetized pony.
J. Apple. Physiol
. 48(1):10-15, 1980.
5. Jonsson, L. O. Predictable PaCO
2
with two different flow settings using the Mapleson D. system.
Acta Anaesthesiol Scand
. 34:237-240, 1990.
6. McKerrow, C. B., and Otis, A. B. Oxygen cost of hyperventilation.
J. Apple. Physiol
. 9:375-79, 1956.
7. Robbins, P. A., Swanson, G. D. and Howson, M. G. A prediction-correction scheme for forcing alveolar gases along certain time courses.
J. Apple. Physiol
. 52(5):1353-1357, 1982.
8. Smith, D. M., Mercer, R. R. and Eldridge, F. L., Servo control of end-tidal CO
2
in paralyzed animals.
J. Apple. Physiol
. 45(1):133-136, 1978.
9. Somers, V. K., Mark, A. L., Zavala, D. C. and Abboud, F. M. Influence of ventilation of hypocapnia on sympathetic nerve responses to hypoxia in normal humans.
J. Appl. Physiol
. 67(5):2095-2100, 1989.
10. Sorkness, R. and Vidruk, E. Reflex effects of isocapnic changes in ventilation of tracheal tone in awake dogs.
Respir. Physiol
. 69:161-172, 1987.
11. Tenney, S. M. and Reese, R. E. The ability to sustain great breathing efforts.
Respir. Physiol
. 5:187-201, 1968.
12. Wahba, R. W. M. and Tessler, M. J. Misleading end-tidal CO
2
tensions.
Can. J. Anaesth
. 43(8):862-6, 1996.
This requires compensating for excess ventilation by inhaling CO
2
either from exhaled gas or some external source. The amount of CO
2
required to be inhaled needs to be adjusted manually or by an automated servo-controlled mechanism, depending on how fine the control of PaCO
2
is required. The input signal is the P
ET
CO
2
. Stability of PaCO
2
depends on the variability of CO
2
production and ventilation on the one hand, and the ability of a system to compensate for this variability on the other.
The termination of the anaesthetic effects of intravenously administered drugs depends on metabolism and redistribution. The recovery time from anaesthesia is therefore determined by the drug's pharmacology and cannot be accelerated.
This is not so for inhaled anaesthetic vapours. The uptake and elimination of anaesthetic vapours is predominantly through the lungs. The partial pressure of an anaesthetic vapour in the blood going to the brain is dependent upon the equilibration of vapour between the blood and the lungs. The concentration of vapour in the lungs in turn is dependent on the concentration of vapour in the inhaled gas, the rate of breathing, and the rate of transfer of gas between the lung and the blood. The newer anaesthetic agents desflurane and sevoflurane have very low blood solubility. Therefore the amount of drug transferred between the lungs and the blood is small and can, for discussion purposes, be ignored. Thus, for a patient waking up from a vapour anaesthetic, the greater the rate of breathing, the more vapour is eliminated from the lungs. However, in anaesthetized patients breathing spontaneously, ventilation is often depressed as a result of combined effects of residual intravenously administered anaesthetic drugs, pain relieving drugs (i.e. narcotics), the effects of surgery, as well as the respiratory depressant effect of the residual anaesthetic vapour itself
Practically, there has been limited scope for intervention to hasten the process of eliminating vapour from the lung and thus hastening the rate of emergence from the effects of vapour anaesthesia.
Proposals in Prior Art
1. Artificial Ventilation
Manually or mechanically hyperventilating patients at the end
Srivastava Virenda
Stetina Brunda Garred & Brucker
Weiss John G.
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