The classification emphasizes that a PCO2 more than 100mmhg is unlikely to occur when a patient is breathing air , since dilution of oxygen in the alveolar gas by the raised carbon dioxide level causes severe hypoxia .
It has also been observed that 100mmhg represents the upper limit of hypoxia which can be compatible with life in patients with severe lung disease .
PARTIAL PRESSURE OF GASES IN ALVEOLI 760mmhg 760mmhg total 47mmhg 47mmhg Water vapor 100mmhg 40mmhg Carbon dioxide 578mmhg 578mmhg nitrogen 35mmhg 95 mmhg oxygen Hypoventilation pco2=100mmhg Normal ventilation Arterial pco2 =40mmhg
Hypercapnic narcosis is associated with marked ventilatory and circulatory stimulation with increased muscle tone and cortical seizure activity.It were these characteristics which finally deterred anaesthetists from their attempts to use co2 as an anaesthetic agent.
There is inhibition of glycolytic pathway and TCA cycle ,but an increase in succinate level.
Decrease delivery of pyruvate from normal glycolytic pathway -> increase use of amino acid as an alternative source of pyruvate ->decreased amino acid pool in the brain and increase in ammonia content due to oxidative deamination-> increased activity of asparate amino transferase ->glutame depletion and increased asparate formation
The degree of brain intracellular Ph disturbance is dependent on the degree of intracellular buffering of the induced change of PaCo2.The regulation of brain Ph is time dependent and for a given sustained level of Ph ,intracellular Ph regulation reaches 90℅ of the theoretical possible value within three hours and thereafter changes are very little.
Three mechanism that contribute to the buffering of intacellular Ph :-
Increased Paco2 and associated acidosis decreases myocardial contractility, heart rate and the contractility of isolated papillary muscle but the effect is short lived and there is progressive recovery of function as the intracellular Ph changes are buffered.
Hypercarbia has a depressant effect on peripheral vascular resistance , mostly on
An elevation of Paco2 (39 -50 mmhg) in conscious patient during controlled or spontaneous ventilation causes marked increases in heart rate , myocardial contractility,consequent increase in cardiac output while SVR is reduced .
The effect of hypercapnia on ventricular performance is dependent on hydraulic impendence to left ventricle .( SVR and the ratio of mean arterial pressure to cardiac output.) Hypercapnia almost associated with marked reduction SVR and the non pulsatile term of aortic input impedance, thus the depressant effect of anaesthesia and CO2 on the ventricular muscle are to some extent offset
Decrease in SVR is most marked in Enflurane , though seen with most anaesthetic .
HYPERCAPNIA, ANAESTHSIA AND β ADRENO RECEPTOR BLOKADE
The main sympathetic effect of hypercania are mediated through adrenergic β receptors
In the presence of β receptor blockade, effects of hypercapnia on sympathetic nervous activity are inhibited , leaving the direct myocardial depressant effects of carbon dioxide to produce additive effects with the anaesthetic agents
Propanolol has a selectivity for peripheral vascular β receptor rather than heart and since it doesn't block ά receptors ,circulating catecholamine exert an unopposed vasoconstrictor effect on systemic blood vessels .Thus combination of hypercapnia ,anaesthesia and β receptor blockade may increase rather than decrease SVR.
So, PACO2 is determined by alveolar ventilation (VA ) and CO2 production (VCO2
But if the inspired gas contains carbon dioxide than the equation will be
FACO2 = FICO2 + VCO2 / VA
When FICO2 approaches FACO2 , constancy of latter is no longer maintained despite an increase in ventilation .The body tends to compromise by tolerating a slight increase in FACO2 rather than increasing alveolar ventilation to the point at which FACO2 is returned to normal.
The relationship between hypercarbia and minute ventilation can also be expressed by following manner
Vm =S(PETco2 – B)
Where Vm is minute ventilation
S is ventilatory sensitivity to CO2
B is apneic threshold
The value of S shows large intra and inter subject variability .Apart from genetic variability the value S depends on sex, female and male sex hormone, age , physical training ,circadian rhythm ,behavioral state ,underlying disease, ambient oxygen tension and acid- base status
In awake human, the conscious drive to breath and other stabilizing influence on respiration maintain breathing, when CO2 tension is below resting value. This results in a flattening of the CO2 response curve at lower CO2 level .This is referred as a dogleg or hockey stick .
When consciousness is lost , as with sleep or anaesthesia apnea occur when there is hypocapnia ; dogleg disappears and a true apneic threshold point is found
An increase in arterial CO2 tension increases ventilation by stimulating both peripheral and central receptors .
Dynamic end- tidal forcing technique was developed to quantify the separate contribution of central and peripheral receptors .This technique shows that peripheral receptors takes 6 secs to react to hypercarbia where as central receptors takes 12 secs to do the same.
In awake patient ,the contribution of peripheral and central receptors to CO2 stimulated ventilation is 30% and 70% respectively .
Hyperdynemic circulation during hypercapnia in an anaesthetized person, transport of oxygen between lung and tissue is enhanced by increased cardiac out put and reflected by lower than normal ateriovenous oxygen content differrence.
Alveolar arterial PO2 difference is reduced due to higher oxygen content in mixed venous blood and less venous admixture
But this slight increase in arterial PO2 is offset by impaired uptake of oxygen by hemoglobin ( bohr effect on oxygen dissociation curve )
The gross displacement of the curve to the right accounts for desaturation of arterial blood despite normal oxygen tension .
Hypercapnia causes increase in pulmonary arterial pressure in most circumstances that is associated with increase pulmonary blood flow. Although Co2 has some direct vasoconstrictor effect , vasoconstriction is mainly due to effect of acid on pre and post capillary vessels .
Hypercapnia increases coronary blood flow which is disproportionate to the increase in the left ventricular work and myocardial O2 requirement .This effect is associated with marked increase in coronary sinus PO2 and consequent decrease in the arteriovenous O2 content difference across coronary circulation
The influence of hypercapnia on pressure flow relationship in the splanchnic and hepatic circulation varies considerably according to anaesthetic drug used
During thiopentone and nitrous oxide anaesthesia sympathetic adrenergic response to hypercarbia are not unduly suppressed , so hypercapnia is associated with splanchnic vasoconstriction and reduced hepatic blood flow
During halothane anaesthesia the balance is such that the vasodilator effect of carbon dioxide promotes splanchnic vasodilatation and marked increase in hepatic blood flow .
Schafer et al observed that during the first 6-12 hours of sustained hypercarbia in response to breathing 15% carbon dioxide , body temperature falls by about 3.c , but recover to the original value in a period of three days .
The reduction of body temperature is due to
Direct inhibition of cellular metabolism .
Increased heat loss due to vasodilator effect of CO2 on skin blood vessels
A transient decrease , followed by a sustained increase in the nor adrenaline content of cells in the hypothalamic region involved in thermoregulation
OBSTRETICS AND NEONATAL IMPLICATION OF HYPERCAPNIA
The generalized circulatory effects of hypercapnia are reflected in changes in both maternal and fetal circulation. With consequent effect on fetal oxygenation
.Ivanko , Elam and Huffman observed that moderate hypercapnia in the human mother during caesarian section is associated with elevated umbilical PO2 .
The kidney compensates for acidosis by excreting H+ ions and retaining bicarbonates .
When there is acute rise in co2 that is not uncommon intra operatively, kidney doesn’t get time for compensation. But in chronic hypercarbia , due to compensatory mechanism arterial Ph is much higher for the corresponding acute change of Pco2