Method of maintaining constant arterial PCO2 and measurement...

Surgery – Respiratory method or device

Reexamination Certificate

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C128S204180, C128S204220, C128S203250, C128S205110, C128S914000

Reexamination Certificate

active

06799570

ABSTRACT:

CROSS-REFERENCE TO RELATED APPLICATIONS
This Application claims priority to Canadian Application Serial No. 2,346,517 filed May 4, 2001.
STATEMENT RE FEDERALLY SPONSORED RESEARCH/DEVELOPMENT
(Not applicable)
BACKGROUND OF INVENTION
The present invention relates to a method to maintain isocapnia when breathing exceeds baseline breathing and a circuit therefor. Preferably, the circuit includes a non-rebreathing valve, a source of fresh gas, a fresh gas reservoir and a source of gas to be inhaled when minute ventilation exceeds fresh gas flow. Preferably the flow of the fresh gas is equal to minute ventilation minus anatomic dead space. Any additional inhaled gas exceeding fresh gas flow has a partial pressure of CO
2
equal to the partial pressure of CO
2
of arterial blood.
Venous blood returns to the heart from the muscles and organs partially depleted of oxygen (O
2
) and a full complement of carbon dioxide (CO
2
). Blood from various parts of the body is mixed in the heart (mixed venous blood) and pumped into the lungs via the pulmonary artery. In the lungs, the blood vessels break up into a net of small vessels surrounding tiny lung sacs (alveoli). The vessels surrounding the alveoli provide a large surface area for the exchange of gases by diffusion along their concentration gradients. After a breath of air is inhaled into the lungs, it dilutes the CO
2
that remains in the alveoli at the end of exhalation. A concentration gradient is then established between the partial pressure of CO
2
(PCO
2
) in the mixed venous blood (PvCO
2
) arriving at the alveoli and the alveolar PCO
2
. The CO
2
diffuses into the alveoli from the mixed venous blood from the beginning of inspiration (at which time the concentration gradient for CO
2
is established) until an equilibrium is reached between the PCO
2
in blood from the pulmonary artery and the PCO
2
in the alveolae at some time during breath. The blood then returns to the heart via the pulmonary veins and is pumped into the arterial system by the left ventricle of the heart. The PCO
2
in the arterial blood, termed arterial PCO
2
(PaCO
2
) is then the same as was in equilibrium with the alveoli. When the subject exhales, the end of his exhalation is considered to have come from the alveoli and thus reflects the equilibrium CO
2
concentration between the capillaries and the alveoli. The PCO
2
in this gas is the end-tidal PCO
2
(P
ET
CO
2
). The arterial blood also has a PCO
2
equal to the PCO
2
at equilibrium between the capillaries and alveoli.
With each exhaled breath some CO
2
is eliminated and with each inhalation, fresh air containing no CO
2
is inhaled and dilutes the residual equilibrated 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
E
), usually expressed in L/min, is exactly that required to eliminate the CO
2
brought to the lungs and establish an equilibrium P
ET
CO
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 carried to the lungs and one then has to breathe harder 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 excess CO
2
is washed out of the alveoli and the PaCO
2
falls.
It is important to note that not all V
E
contributes to elimination of CO
2
. The explanation for this is with reference to the schematic in the lung depicted in FIG.
10
. The lung contains two regions that do not participate in gas equilibration with the blood. The first comprises the set of conducting airways (trachea and bronchi)
100
that act as pipes directing the gas to gas exchanging areas. As these conducting airways do not participate in gas exchange they are termed anatomic dead space
102
and the portion of V
E
ventilating the anatomic dead space is termed anatomic dead space ventilation (V
Dan
). The same volume of inhaled gas resides in the anatomic dead space on each breath. The first gas that is exhaled comes from the anatomic dead space and thus did not undergo gas exchange and therefore will have a gas composition similar to the inhaled gas. The second area where there is no equilibration with the blood comprises the set of alveoli
103
that have lost their blood supply; they are termed alveolar dead space
104
. The portion of V
E
ventilating the alveolar dead space is termed alveolar dead space ventilation (V
Dalv
). Gas is distributed to alveolar dead space in proportion to their number relative to that of normal alveoli (normal alveoli being those that have blood vessels and participate in gas exchange with blood). That portion of V
E
that goes to well perfused alveoli and participates in gas exchange is called the alveolar ventilation (V
A
). In
FIG. 10
, the numeral references
105
and
106
indicate the pulmonary capillary and the red blood cell, respectively.
Prior art circuits used to prevent decrease in PCO
2
resulting from increased ventilation, by means of rebreathing of previously exhaled gas are described according to the location of the fresh gas inlet, reservoir and pressure relief valve with respect to the patient. They have been classified by Mapleson and are described in Dorsch and Dorsch pg 168.
Mapleson A
The circuit comprises a pressure relief valve nearest to the patient, a tubular reservoir and fresh inlet distal to the patient. In this circuit, on expiration, dead space gas is retained in the circuit, and after the reservoir becomes full, alveolar gas is lost through the relief valve. Dead space gas is therefore preferentially rebreathed. Dead space gas has a PCO
2
much less than PaCO
2
. This is less effective in maintaining PCO
2
than rebreathing alveolar gas, as occurs with the circuit of the present invention.
Mapleson B and C
The circuit includes a relief valve nearest the patient, and a reservoir with a fresh gas inlet at the near patient port. As with Mapleson A dead space gas is preferentially rebreathed when minute ventilation exceeds fresh gas flow. In addition, if minute ventilation is temporarily less than fresh gas flow, fresh gas is lost from the circuit due to the proximity of the fresh gas inlet to the relief valve. Under these conditions, when ventilation once again increases, there is no compensation for transient decrease in ventilation as the loss of fresh gas will prevent a compensatory decrease in PCO
2
.
Mapleson D and E
Mapleson D consists of a circuit where fresh gas flow enters near the patient port, and gas exits from a pressure relief valve separated from the patient port by a length of reservoir tubing. Mapleson E is similar except it has no pressure relief valve allowing the gas to simply exit from an opening in the reservoir tubing. In both circuits, fresh gas is lost without being first breathed. The volume of gas lost without being breathed at a given fresh flow is dependent on the pattern of breathing and the total minute ventilation. Thus the alveolar ventilation and the PCO
2
level are also dependent on the pattern of breathing and minute ventilation. Fresh gas is lost because during expiration, fresh gas mixes with expired gas and escapes with it from the exit port of the circuit. With the present invention, all of the fresh gas is breathed by the subject.
There are many different possible configurations of fresh gas inlet, relief valve, reservoir bag and CO
2
absorber (see Dorsch and Dorsch, pg. 205-207). In all configurations, a mixture of expired gases enters the reservoir bag, and therefore rebreathed gas consists of combined dead space gas and alveolar gas. This is less efficient in maintaining PCO
2
constant than rebreathing alveolar gas preferentially as occurs with our circuit, especially at small increments of V above the fresh gas flow.
BRIEF SUMMARY OF THE INVENTION
The present invention comprises a method and a circuit that maintains a constant PCO
2
More particularly, the present invention maintains a constant PC

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