Acids and Bases Flashcards
normal pH of arterial blood
7.38-7.43
normal pH of venous blood
7.32-7.38
(slightly more acidic due to increased CO2 content)
acidemia
[H+] rises so pH drops below 7.38
alkalemia
[H+] falls so that pH breaches 7.43
Respiratory Acidosis and Alkalosis Basis
- Respiration exchanges CO2 for O2
- CO2 generated via metabolism is carried in blood as HCO3-, cabaminohemoglobin and protonated hemoglobin
- CO2 is directly coupled to H+ via the HCO3- buggering system
- therefore, changes in ventilation can lead to an acid-base imbalence
- altered ventilation can be used to compenstate for certain acid-base disturbances
Respiratory Acidosis
- results from impaired ability to expire CO2
- since CO2 = H+ load,
- pH decreases as plasma CO2 (ie: PCO2) rises above normal
- pH < 7.38 = acidemia
- can be caused by resistance of diffusion barrier at the level of the alveolus and/or an abnormally decreased RR –> hypercapnia
- can result from inhibition of the medullary respiratory center (drugs, cardiac arrest), pathologies of respiratory muscles/chest wall, disordrs affecting gas exchange (severe asthma, pneumonia, chronic obstructive pulmonary disease)
hypercapnia
excessive carbon dioxide in the bloodstream, typically caused by inadequate respiration.
Acute Respiratory acidosis
“Up 1 for 10”
1 meq/L increase in HCO3- per 10 mm Hg
increase in PCO2 is predicted
Common causes: obstructive sleep apnea, aspiration of foreign body/vomitus, laryngospasm
Within red blood cells (RBCs)
- increase in PCO2, the buffering equation is driven to the right –> resulting in an increase in both H+ and HCO3-
- this affords some immediate buffering.
- Additional H+ is buffered by intracellular mechanisms:
- mediated by the swap of extracellular H+ for intracellular K+
- Erythrocytes provide HCO3-
- following the inward diffusion of CO2, and through the exchange of extracellular Cl- for intracellular HCO3-
- sodium lactate buffering:
- Na lactate + H2CO3 → NaHCO3 + lactic acid
- Within cells, this lactic acid can be metabolized into CO2 + H2O or enter the gluconeogenic pathway for the production of glucose.
Chronic Respiratory Acidosis
a 4 meq/L rise in HCO3- per 10 mm Hg increase in PCO2 is predicted
- 4-5 days of respiratory acidosis (i.e. chronic respiratory acidosis), the kidneys respond with increased H+ excretion
- H+ excretion not only removes H+, but remarkably equates to enhanced renal HCO3 production and retention
Respiratory Alkalosis
results from pathologic increase in respiratory drive
- lowers pCO2 with resultatnt increase in pH (>7.43)
- Compenstation: plasma biarb must be reduced to lower pH toward the normal range
- Acute compensation
Respiratory Alkalosis
- results from pathogenic incease in respiratory drive
- lowers PCO2, with resultant increase in pH (>7.43)
- Compenstation: plasma HCO3- must be reduced to lower pH toward the normal range
- note: alkalinity is an increase in pH, meaning relatively low [H+]
- thus: favorable gradient for H+ to leave cells
Acute Respiratory Alkalemia
Metabolic acidosis
characterized by a fall in plama HCO3- and low pH
-
loss of HCO3- and/or the buffering of a non-carbonic acid:
- lactic acidosis; ketoacidosis
- alcoholism
- acute/chronic kidney disease
- CI HCO3- loss
- Ingestions: aspirin, methanol, ethylene glycol
(pH < 7.38) results from
1) the inability of the kidneys to handle the dietary
acid load,
2) an increase in plasma [H+], and/or
3) a decrease in plasma [HCO3-]
What condition would abnormally low pH, low HCO3-, and lower than normal PCO2 indicate?
Matabolic acidosis
