Wall: Acid-Base Flashcards
What are the two categories of acids?
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Carbonic: volatile, can be converted to CO2 (about 15,000 mmol/d) -> eliminated by the lungs
1. CO2 is an acid b/c we are 60% water
2. Carb + fat metabolism = CO2 -
Non-carbonic: non-volatile acids, like phosphoric H3PO4 and sulfuric, H2SO4 (50-100 mEq/d) -> combine with buffers, then excreted by the kidney
1. Fixed acids that can’t be converted to carbonic acid (protein + phospholipid metabolism)
2. Job of the kidney to regenerate the bicarbonate used up in buffering these
What is an acid? Base?
- Acid: can donate H+
- Base: can accept H+
What is the clinical pH range?
- 6.80-7.80 (H+ conc. b/t 16-160 nEq/L
- Arterial blood gas machine measures CO2, pH, and O2 in arterial samples
- Bicarbonate can be calculated via Henderson equation
- Highly regulated in body b/c virtually all enzymes, proteins have pH-dependent functions
How do we calculate the plasma bicarbonate concentration? What is normal?
- Labs measure total CO2 concentration -> dissolved carbon dioxide plus bicarbonate concentration; ~25-26 meq/l in venous samples
- Due to this technique, total CO2 conc. exceeds plasma bicarbonate concentration by 1.0 to 1.5 mEq/L
- Normal plasma bicarbonate concentration is approximately 24 mEq/L
What are acidemia and alkalemia?
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Acidemia: reduced pH, or elevated H+ concentration
1. Acidosis: process that lowers pH -
Alkalemia: increased pH, or reduced H+ conc.
1. Alkalosis: process that elevates pH - NORMAL HUMAN pH = 7.4
What is the bicarbonate buffer system formula?
IMPORTANT!!!
CO2 + H2O = H2CO3 = H+ + HCO3-
- If closed sytem, pKa = 6.1 (weak acid); normal pH = 7.4
- We are an open system via the lungs excreting CO2, making this system a highly efficient buffer
- Bicarbonate is the major EC buffer
What is the only way to change the pH in the body?
- By changing:
1. PaCO2 (dissolved = CO2 + H2O) or
2. HCO3-

How do we calculate H+? From pH?

- H+ = 24 (CO2/HCO3-)
- pH must be converted to H+ (nEq/L)
1. pH = 7.4 = 40 nEq/L - 7.40 = 40 = 24 (40/24)
1. Overall, H+ = 80 - decimal digits of pH (more or less)
What are the normal pH, pCO2, and HCO3- values?
- pH = 7.35 - 7.45 (7.40) = -log(H+)
1. [H+] = 24 x pCO2/HCO3- - pCO2 = 36-44 mmHg (40 mmHg)
- HCO3- = 22-26 mEq/L = 24 mEq/L
What are metabolic disorders?
- Processes that directly alter bicarbonate concentration
1. Metabolic acidosis: decreased bicarbonate (increased H+)
2. Metabolic alkalosis: increased bicarbonate
What are respiratory disorders? What is the buffer effect?
- Processes that directly alter CO2
1. Respiratory acidosis: increased CO2
2. Respiratory alkalosis: decreased CO2 - Buffer effect: slightly increased HCO3- with respiratory acidosis -> slightly decreased HCO3- with respiratory alkalosis
What is buffering?
- Prevents wide changes in pH in response to the addition of acid or base
- Bicarbonate: major EC buffer (can be easily measured); there are also IC buffers
- Buffers attenuate changes in pH in response to acid-base disorders -> immediate onset
- Isohydric principle: all buffers change in the same direction
What is the purpose of the acid-base system? What are the 4 key buffer pairs?
- To maintain normal pH via buffer systems: H+ donor and acceptor
- Bicarbonate (ECFV): HCO3-, H2CO3
- Phosphate (urine): H2PO42-, H2PO4
- Ammonia (urine): NH3, NH4+ (can be metabolically regulated by the kidney)
- Protein: protein, protein (IC buffer)
- NOTE: we need something more than buffers b/c we want a whole body response (secondary mechanisms)
What are secondary (compensatory) mechanisms?
- Additional physiologic responses that occur in response to changes in pH -> move back toward normal, but never completely correct
- INVARIABLY PRESENT in simple acid-base disorders (if not present, it is a mixed disorder)
What are the compensatory mechanisms for metabolic and respiratory disorders?
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Metabolic disorders: respiratory system compensates by altering CO2 -> via lungs
1. Hyperventilation
2. Rapid onset: minutes -
Respiratory disorders: compensation via alterations in bicarbonate concentration -> via kidney
1. Slower onset: 1-2 days (there will be difference b/t acute and chronic disorders b/c this response takes longer)
What are 4 important mechanisms that buffer an acid load?
- Buffer systems (primarily bicarbonate) -> EC fluid -> immediate (H+ + HCO3- = H2CO3 = H2O + CO2)
- Increased rate and depth of breathing to decrease CO2 -> via lungs -> minutes to hours
- Buffer systems (bicarbonate, phosphate, protein) -> IC fluid -> 2-4 hours
- H+ excretion, H2CO3- reabsorption, bicarb generation -> kidneys -> hours to days
Summarize how the 4 disorders affect pH, HCO3-, and pCO2.
- Metabolic acidosis: DEC, DEC, DEC (compensatory)
- Metabolic alkalosis: INC, INC, INC (compensatory)
- Resp. acidosis: DEC, INC (compensatory), INC
- Resp. alkalosis: INC, DEC (compensatory), DEC
- NOTE: it is far more difficult to stop breathing than to increase it, so lung response to metabolic acidosis much more precise than that to metabolic alkalosis
1. Notice trends above to aid in memorization
What are the golden rules for simple acid-base disorders?
- PCO2 and HCO3 always change in the same direction
- Secondary physiologic compensatory mechanisms must be present (if not present, it’s a mixed disorder)
- Compensatory mechanisms never fully correct pH (bring it back to normal, but never fully correct or overshoot)
- NOTE: if any of these rules are violated, you know it is mixed, and there is more than one disorder going on simultaneously
What is metabolic acidosis? Etiology?
- Process that reduces plasma bicarbonate conc.
- Etiology:
1. Decreased renal acid excretion (renal tubular acidification defect)
2. Direct bicarbonate losses (GI tract, urine): prox tubule problem (where most H2CO3 reabsorbed) or gastric secretion
a. Drugs that inhibit carbonic anhydrase in renal tubule (acetazolamide: glaucoma tx)
3. INC acid generation (exogenous or endogenous) -> only 2 clinically common endogenous acids are:
a. Lactic acidosis (shock, oxygen debt)
b. Ketoacidosis (starvation, type 1 diabetic)
What are the 3 causes of metabolic acidosis?
- INC acid generation: lactic acidosis, ketoacidosis, ingestion of acids (ASA, ethylene glycol - suicide attempts, methanol w/alcohol), dietary protein intake (animal source)
- Loss of bicarbonate: GI (diarrhea, intestinal fistulas), renal (type 2 prox renal tubular acidosis)
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Decreased acid excretion (impaired ammonium excretion): renal failure (DEC GFR), type 1 distal renal tubular acidosis, type 4 renal tubular acidosis (hypoaldosteronism -> not pumping enough H+ ion into urine in exchange for K+, so also hyperkalemia)
1. Defect in H+ pumps could be congenital
2. Chronic kidney disease: less nephrons working
What is respiratory acidosis?
- Induced by hypercapnia (decreased alveolar ventilation): CO2 retention
- Buffering mechanisms raise plasma bicarbonate concentration (rapid, but limited response: 1-2 mEq/L)
- Kidney minimizes change in EC pH by increasing acid excretion (NH4+), generating new bicarbonate ions (delayed response: 2-3 days)
What are some of the causes of respiratory acidosis?
- Acute: something that creates hypoxemia or blocks your airway
- Chronic: COPD

What is respiratory alkalosis?
- Reduced CO2 due to increased alveolar ventilation: blown off too much CO2
- Buffering processes lower plasma bicarbonate conc (rapid, but limited response: 1-2 mEq/L)
- Kidney response is to reduce net acid excretion: elim bicarbonate into the urine, or decrease ammonium secretion -> delayed response: 1-2 days
What are some of the causes of respiratory alkalosis?
- Anything that injures the brain, or causes you to be hypoxic, provoking hyperventilation














