Gaz du sang

Acidose, Acidose Métabolique, Acidose Respiratoire,

Alcalose, Alcalose Métabolique, Alcalose Respiratoire

Le pH qui résulte de l'équilibre entre les acides et les bases (alcalins).

Deux effecteurs maintiennent le pH normal: Rein et Poumon.

Une perturbation de l'état acido-basique (désordre primaire) de l'un entraine une action compensatrice de l'autre, parfois insuffisante.

Analyse immédiate ou conservation (2h max) dans de la glace.

C'est grave quand??? Extrèmes?

1 kPa = 7.5006375541921 mmHg

PaO2 normale > 80 mmHg (10,7 kPa) mais dépend de l'age. 60 mmHg = 8 kPa.
pH:

normales: 7,35 à 7,45 (7.2: acidose sévère)
The pH is the negative logarithm of the hydrogen ion concentration. When the pH changes by 0.3 units, e.g., from 7.4 to 7.1 the hydrogen ion concentration doubles (from 40 to 80 nmol/l).
In the interests of clear thinking remember that, at body temperature, true neutral is pH 6.8. So, nearly all acid-base results deal with a patient whose plasma is actually on the alkaline side of neutral. Nevertheless, "Acidemia"is a useful shorthand for "...more acid than the normal pH of 7.4". A patient with a pH of 7.33 has blood on the alkaline side of neutral but, being on the acid side of normal, is acidemic. If his PCO2 is 60 he has a respiratory acidosis with a compensating metabolic alkalosis of 6 mEq/L.

PaCO2:
- normales: 35 à 45 mmHg (4,7 – 6 kPa)
- Carbon dioxide is respiratory acid - it is the only acid which can be exhaled via the lungs. Strictly speaking carbon dioxide is a gas, not an acid. Carbonic acid is only formed when combined with water. Nevertheless, clinicians customarily regard carbon dioxide and respiratory acid as synonymous. If you want to sound like a doctor - a High PCO2 is the same as Respiratory Acidosis and vice versa.
- À noter qu’une mesure de PCO2 de sang veineux, plus facile et moins douloureuse à obtenir, inférieure à 45 mmHg exclut l'hypercapnie [source].
- Voir aussi use of venous-to-arterial carbon_dioxide tension difference to guide resuscitation therapy in septic shock.
Tout ce petit monde est lié: HCO3 = k x PCO2/H
HCO3-: CO2T:
- normales: 23 à 27 mmol/l
- The belief that bicarbonates measures metabolic acidosis arises because, in a patient with no respiratory abnormality, the bicarbonate does reflect the metabolic disturbance. However, the bicarbonate level is varied by both components, respiratory and metabolic. It cannot, therefore, be an ideal measure of either. Moreover, the relationship between metabolic acidosis and bicarbonate is neither consistent nor linear. And, finally, in acid-base determinations the concentration (in mEq/L) of the bicarbonate ion (HCO3-) is not measured, it is calculated from the PCO2 and pH. Bicarbonate is neither an ideal measure of metabolic acidosis nor a measure of respiratory acidosis. This is because both the respiratory and the metabolic components can affect the concentration of bicarbonate ions. The exception to this rule would be when the only results available are from Blood Chemistry analysis and the patient appears to have normal lungs. Here, a bicarbonate change almost certainly indicates a metabolic abnormality. When Standard Base Excess (SBE) is available, which it is in acid-base balance measurements, it is the best measure of the metabolic disturbance.
Standard Base Excess SBE is the Base Excess value calculated for anemic blood (Hb = 5 g/dl) on the principle that this closely represents the behavior of the whole human being. Base Excess as a better method of measuring the metabolic component. In essence the method calculated the quantity of Acid or Alkali required to return the plasma in-vitro to a normal pH under standard conditions. The pH is always determined by the two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the PCO2, i.e., any change in the pH unexplained by the PCO2 indicates a metabolic abnormality. Standard Base Excess is the best overall measurement we have of the level of the metabolic acidosis. Metabolic acidosis is described as a "negative" base excess.

Selon [Numn 1977] les extrèmes de la PaO2 sont:

20-30 ans: 84 - 104 mmHg
30-40 ans: 81 - 101 mmHg
40-50 ans: 78 - 98 mmHg
50-60 ans: 74 - 94 mmHg
60-70 ans: 71 - 91 mmHg

aprés 60 ans: PaO2 moy = 100.1 - age x 0.323

à ramener à la FiO2 en calculant Pa02/FiO2: bas sous 300 (= sous air une PaO2 de 63), trés bas sous 200 (= sous air une PaO2 de 44 On est dans la valeur veineuse là !!!). La normale est de 95/0,21= 453. (Rem perso: à part l'air ambiant (21%) et la VNI (100%) on ne voit pas comment connaitre les FiO2 intermédiaires...)

PaO2 + PaC02 > 130 If the sum of PO2 + PCO2 is greater than expected, then the analysis contains an error. A sum which is smaller suggests that the lungs are failing to adequately transfer oxygen. With nitrogen and water vapor "fixed", oxygen and carbon dioxide share the remaining space. With normal lung function and accurate analysis, the arterial blood gas values reflect this.

Situation cliniques

Perturbations initiales:

Vomissements ou aspiration:
- perte d'acide (HCl): alcalose métabolique
- HypoK par perte urinaire due à l'alcalose (?)
Diarrhée: perte de bases (bicarbonates):
- acidose métabolique,
- perte de K (masquée par l'acidose créée par la perte de base, qui fait sortir le K des cellules)
Diarrhée + Vomissements: les gaz peuvent être normaux alors que le patient est en alcalose métabolique + acidose métabolique: valeur du trou anionique (normal ici) et de l'hémoconcentration lors de l'analyse des gaz du sang...
desH2O: The pH of the normal mixture of electrolytes in the extracellular fluid (7.4) is relatively alkaline compared to neutral pH at body temperature (6.8). When this electrolyte mixture is concentrated by dehydration, the relative alkalinity is more marked and the pH is further away from neutral. Rehydration is the obvious therapy.
Dilution: Diluting the normal slightly alkaline mixture of extracellular electrolytes, also dilutes the alkalinity. This moves the pH closer to neutral at body temperature (6.8)Diuresis, physiological or therapeutic, is the required therapy.
Apports alimentaire et son catabolisme: apport d'acides
Ins. rénale:réduit (voir abolit en cas d'anurie) l'excrétion acide ou alcaline d'adaptation: une anomalie métabolique (quelle que soit la cause) n'apparait que si le rein est lésé:
- rétention d'acides fixes: une clairance de Créat < 30 ml/mn entraine constament une Acidose Métabolique avec une augmentation habituellt modérée des anions indosés jusqu'à 25 mmol/l.
- Une desH20 (Urée>créat) l'aggrave
Etat de choc => Ins. rénale + production d'acide lactique =>Acidose Métabolique, effet shunt pulmonaire pas poumon de choc? (abaisse la capnie)
Carence en Insuline chez le diabétique => acidose métabolique
Détresse respiratoire: augmentation du CO2 acide. Gravité max si associée à une ins. rénale.
Embolie pulmonaire : alcalose respiratoire
Hypotension : acidose métabolique
Cirrhose : alcalose respiratoire
Sepsis: alcalose respiratoire et acidose métabolique
Diurétiques : alcalose métabolique
BPCO : acidose respiratoire
Demonstrations by Xu et al that the body and brain tolerate pH values as low as 6.2 without damage provided circulation and oxygenation are maintained. The implication of these results is that an abnormal acid-base value is best regarded as an indicator of trouble, not as pathology in its own right.

ex:

apports alimentaires + ins rénale =>Acidose Métabolique

Compensations

Rapid Respiratory Compensation. The power of the lungs to excrete large quantities of carbon dioxide enables them to compensate rapidly. Unless the respiratory system is diseased or depressed, metabolic disturbances stimulate a prompt response, i.e., metabolic acidosis and metabolic alkalosis normally elicit prompt partial respiratory compensation. Slow Metabolic Compensation. The smaller capacity of the kidneys corresponds to a relatively slower rate of compensation; a patient can be ventilated at an abnormal PCO2 for a day or two before the characteristic, partial compensation is achieved. In the operating room and in the emergency room, therefore, an abnormal PCO2 is not usually associated with a metabolic "compensation". It follows that when a metabolic acidosis or alkalosis is detected, it usually reflects either a separate metabolic disturbance or compensation for a chronic respiratory problem.

Alcalose

Fait rentrer le K dans la cellule
Favorise la fuite urinaire du K

Alcalose respiratoire
Alcalose métabolique

Acidose

Et HypoK: L'acidose fait sortir le K des cellules: Att si K normal ou pire abaissé: c'est une déplétion masquée... (cas dans l'acidocétose)
Une Acidose aiguë libére du Ca de l'Alb => augm du Ca ionisé sans modification du Ca total. Aprés intervention des hormones calciotropes, le Ca ionisé revient à la normale et le Ca total diminue.

[URGENCES 2011] L'acidose s'accompagne d'hyperkaliémie préférentiellement dans les acidoses métaboliques hyperchlorémiques (sortie de potassium de la cellule pour maintenir l'électroneutralité extracellulaire imposée par la non pénétration du chlore) plus que dans les acidoses organiques (électroneutralité extracellulaire préservée en raison de la pénétration intracellulaire concomittante de l'anion organique avec un proton) ou respiratoires.

Acidose Métabolique
Acidose Respiratoire

Sources

http://acid-base.com/
Goulon, Les Urgences