Acid Base 1A Flashcards
Physiologic acids originate from the metabolism of:
- fats and carbohydrates (H2CO3)
- protein (H2PO4; H2SO4)
Carbonic acid (H2CO3) is a product of:
metabolism of fats and carbohydrates
Steps in the formation of carbonic acid (H2CO3) from the products of fat and carbohydrate metaboilism:
(Equation)

What enzyme catalyzes the formation of H2CO3 from CO2 and H2O?
carbonic anhydrase (CA)
Products of protein metabolism/oxidation of sulfur-containing AAs:
- H2PO4-
- H2SO4-
ALSO BUFFERED BY BICARBONATE
Equation for determining physiologic plasma pH:
pH = 6.1 + log([HCO3-]/0.03PCO2)
Plasma pH is derived from the ratio of what two molecules?
- HCO3- : PCO2
- pH = 6.1 + log([HCO3-]/0.03PCO2)
Plasma pH is dependent on what two molecules?
- HCO3-
- PCO2 (CO2)
Normal arterial blood pH range:
7.38 - 7.44
Abnormally elevated pH level and associated condition:
>7.44
alkalemia
Abnormally low pH level and associated condition:
<7.38
acidemia
The four primary acid-base perturbations:
- respiratory acidosis
- respiratory alkalosis
- metabolic acidosis
- metabolic alkalosis
Acid-base perturbations can exist singly or as combined pathologies. What is the only impossible combination?
respiratory alkalosis with respiratory acidosis
Metabolic and respiratory acid-base disorders result from:
Blood HCO3- and/or PCO2 imbalances
Normal compensation for a metabolic acid-base disorder (metabolic acidosis or metabolic alkalosis):
Lungs blow-off or retain CO2
Normal compensation for a respiratory acid-base disorder (respiratory acidosis or respiratory alkalosis):
- Kidneys alter HCO3-, H+, K+ reabsorption or excretion
Derangements in plasma pH are usually caused by:
- an underlying condition.
- underlying condition needs to be corrected in order to resolve acid-base imbalance.
Morbidity and mortality of acid-base disorders depends on:
- the risk associated with underlying disorder causing the acid-base imbalance.
Respiratory acidosis results from:
- impaired ability to expire CO2.
- CO2 equates with H+ load, pH decreases as plasma CO2 (i.e. PCO2) rises above normal.
Hypercapnia is:
- excessive carbon dioxide in the bloodstream.
- typically caused by inadequate respiration.
A nonvolatile acid (fixed acid) is:
- an acid produced in the body from sources other than carbon dioxide.
- not excreted by the lungs.
The nonvolatile acids are excreted by:
the kidneys
All acids produced in the body are nonvolatile except:
- carbonic acid, which is the sole volatile acid.
- excreted as CO2 by lungs.
Charge of fixed (non-volatile) acids:
- Net negative charge; anionic.
- Buffered by renal HCO3- retention and H+ secretion.
The endogenous buffering time line:
- Seconds: plasma and interstitial bicarbonate buffers H+.
- Minutes: bone & intracellular buffers buffer H+.
- Hours: interstitium and plasma cells swap extracellular H+ for intracellular K+.
- Several hours: changes in ventilation.
- Days: kidneys mediate H+ excretion and increase bicarbonate secretion.
Normal plasma bicarbonate (HCO3-) level:
24 meq/L.
Normal plasma PCO2 level:
40 mm Hg.
Acidemia can be caused by either:
- increased PCO2 (respiratory)
- decreased HCO3- (metabolic)
Draw algorithm to determine whether respiratory or metabolic acidemia.

Alkalemia can be caused by either:
- decreased PCO2 (respiratory)
- increased HCO3- (metabolic)
Draw algorithm to determine whether respiratory or metabolic alkalemia.

Two ways RBCs remove/carry CO2:
- CO2 diffuses through the plasma membrane of a RBC, and:
- CO2 + H2O (CA catalyzed) → H2CO3 → H+ + HCO3-.
- HCO3- swapped out of RBC for extracellular Cl-.
- H+ build-up causes conformational change in Hb.
- H+ binds to deoxyHb.
- CO2 diffuses through the plasma membrane of a RBC, and directly binds to deoxyHb to form carboxyhemoglobin.
Steps in how RBCs release oxygen and HCO3- into plasma:
- CO2 diffuses through the plasma membrane of a RBC, and:
- CO2 + H2O (CA catalyzed) → H2CO3 → H+ + HCO3-.
- HCO3- swapped out of RBC for extracellular Cl-.
- H+ build-up causes conformational change in Hb. Oxygen released into plasma.
- H+ binds to deoxyHb.
Normal respiratory rate (resting adult):
16/min
Tachypnea:
elevated respiratory rate (>16/min)
Bradypnea:
depressed respiratory rate (<16/min)
Process of CO2 expiration at alveolus:
- RBC gets to alveolus. Oxygen diffuses into RBC.
- Increased oxygen tension in RBC causes hemoglobin conformation change from deoxyhemoglobin to oxyhemoglobin:
- HHb + O2 → O2Hb + H+ → H+ + HCO3- → H2CO3 → H2O + CO2 (expired)
- CO2Hb → O2Hb + CO2 (expired)

The two rightward reactions in RBCs at the alveoli that lead to CO2 expiration:
- HHb + O2 → O2Hb + H+ → H+ + HCO3- → H2CO3 → H2O + CO2 (expired)
- CO2Hb → O2Hb + CO2 (expired)
Steps in how decreased ventilations lead to respiratory acidosis:
- Less CO2 blown-off.
- Hypercapnia occurs.
- Increased CO2 impedes the rightward reaction in RBC at alveoli.
- Plasma [H+] increases.
- High plasma H+ leads to low pH.
- Respiratory acidosis.
Draw algorithm for determining whether compensated or non-compensated respiratory acidosis:
- respiratory acidosis
- low pH + high PCO2 (> 40)

Compensation rule one: acute respiratory acidosis:
HCO3- up 1 unit for every PCO2 up 10 units
Compensation rule two: chronic respiratory acidosis:
HCO3- up 4 units for every PCO2 up 10 units
Steps in how increased ventilations lead to respiratory acidosis:
- More CO2 blown-off.
- Reaction in RBCs at alveoli driven to the formation of CO2 + H2O.
- Plasma H+ lost as H2O.
- Low H+ leads to elevated pH.
- Respiratory alkalosis.

Draw algorithm for determining whether compensated or non-compensated respiratory alkalosis:
- respiratory alkalosis:
- high pH + low PCO2

Compensation rule three; acute respiratory alkalosis:
HCO3- down 2 for PCO2 down 10
Compensation rule four; chronic respiratory alkalosis:
HCO3- down 5 for every PCO2 down 10
The four respiratory compensation rules:
- Acute respiratory acidosis: “Up 1 for 10”
- Chronic respiratory acidosis: “Up 4 for 10”
- Acute respiratory alkalosis: “Down 2 for 10”
- Chronic respiratory alkalosis: “Down 5 for 10”