Clinical Chemistry: Acid Base Balance Flashcards


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Clinical Chemistry
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1

acid

substance that yields a hydrogen ion when dissolved in water

2

base

substance that yields hydroxyl (OH-) ions

3

pKa

pH in which protonated and unprotonated forms are present in equal concentrations (equilibrium); equal to -log10 the negative log of the ionization constant (dissociation constant); at 37C is 6.1-a constant measured in the lab

4

buffer

a system that resists changes in pH through changes in H+ ions; combination of weak acid or weak base and its salt; in plasma bicarbonate and carbonic acid comprise the major extracellular buffering system

5

acid-base balance

maintenance of hydrogen ions that is highly regulated and controlled; normal in ECF is 36-44 mmol/L at a pH of 7.34-7.44

6

acidosis

a pH level below 7.34 reference range

7

alkalosis

a pH level above 7.44 reference range

8

bicarb buffer system

cell metabolism = acids -> CO2 mixes with H2O to form H2CO3 while H+ are binding with buffer forming carbonic acid -> blood filters through kidneys -> H2CO3 dissociates into HCO3 and H+ again back into the blood stream -> H+ neutralized by hemoglobin buffer system and excreted as part of ammonium while kidneys conserve HCO3 and make NH4 for excretion and excess H+ are released in urine -> HCO3 acts as buffer due to lost H+ -> acids form H2CO3 so more acid is present and less buffer -> carbonic acid goes to lungs and dissociates into CO2 and water for CO2 expiration

9

pulmonary bicarb buffer

O2 inspired -> diffuses from alveoli into blood -> O2 replaces H+ on Hgb -> H+ combine with HCO3 to form H2CO3 to dissociate into CO2 and H2O -> CO2 diffuses into alveoli from blood and is eliminated

10

lungs

first responders of homeostasis in acid base balance; CO2 value in lungs is approximate to HCO3 value in plasma

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hypoventilation

lung reaction to decreased CO2 elimination

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hyperventilation

lung reaction to increased CO2 elimination

13

renal bicarb buffer

reabsorbs HCO3 from glomerular filtrate and secretes H+ in collecting duct in exchange for Na+; helps prevent excessive acid gain in blood due to loss of HCO3 in urine; H+ combine with HCO3 to form H2CO3 which dissociates; HCO3 enters bloodstream, H2O and CO2 enter renal tubule to again reform H2CO3

14

phosphate buffer

urinary buffer that controls pH through urine and ICF; H2PO4 weak acid, HPO4 weak

15

protein buffer system

R-COOH groups on proteins or amino acids donate H+ to lower pH; free amino groups NH2-R accept H+ to raise pH

16

hemoglobin buffer

slow process of about 2-4 hours; important for carbonic acid buffering; can reversibly bind H+ or O2

17

pCO2

partial pressure exerted by dissolved CO2; measured value; amount of H2CO3 is proportional to pCO2

18

HCO3

can be calculated based on H2CO3; total CO2 - (pCO2 x 0.03) (0.03 is the solubility constant for CO2); healthy individuals: HCO3:H2CO3 ratio of 20:1 results in 7.4 pH

19

pO2

partial arterial pressure of oxygen; state of arterial respiration

20

TCO2

total CO2: dissolved HCO3 + H2CO3 + CO2

21

pH= 6.1(pK) + log(base-HCO3/0.0307-solubiility constant x weak acid-H2CO3)

Henderson-Hasselback Equation

22

carboxyhemoglobin

200x binds to hemoglobin 200x stronger than oxygen

23

methemoglobin

unable to bind O2 because iron is an oxidized/ferric state rather than reduced state Fe2+

24

increased H+

lowers attraction of oxygen to hgb

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partial pressure

the amount of gas present in the gas mixture

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(760-atmospheric pressure at sea level - humidity) x percent oxygen gas content

PO2 equation

27

Bohr effect

the effect of pH on hgb O2 affinity; O2 affinity controlled by 2,3 BPG which is produced by anaerobic glycolytic pathway-fluctuates with pH

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high pH

causes accumulation of 2,3 BPG

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low pH

causes synthesis of 2,3 BPG

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Bohr effect in bloodstream

in the bloodstream hgb releases four O2 molecules -> binds four H+ -> adds CO2 and two H+ -> decrease in pH favors release of O2

31

Bohr effect in lungs

in the lungs hgb releases CO2 and two H+ -> hgb adds four O2 molecules -> basic pH of lungs favors uptake of O2

32

decreased affinity

O2 is ready for release, curve shifts right, hgb releases O2, high p50, pH decreased, 2,3 BPG increased, temperature increased, CO2 increases

33

increased affinity

hgb retains O2, curve shifts left, low p50, pH increased, 2,3 BPG decreased, temperature decreased

34

shape of oxygen-dissociation curve and affinity of hgb for O2

affected by hydrogen ion activity, pCO2 and CO levels, body temperature, and 2,3 BPG

35

oxygen saturation, calculated SO2

ratio of O2 bound to hgb compared to total amount of hgb capable of binding O2; normal 96-100%

36

oxygen saturated SpO2

assessed by transcutaneous means such as pulse oximetry

37

PaO2

normally 75-100 mm Hg; state of arterial respiration; reflects normal gas exchange, decreases with age and loss of elasticity within the lungs; low indicates hypoxia

38

arterial pressure of CO2

carbon dioxide levels are expressed as PaCO2; p is the partial pressure of the gas dissolved in the blood; normal 35-45 mmHg; reflects the state of arterial ventilation-decreased in hyperventilation (rapid breathing, more rapid loss of CO2); acute, sudden changes will alter the pH

39

acidosis

excess acid or H+ resulting in pH <7.34

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alkalosis

excess base or HCO3 resulting in pH >7.44

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7.4

normal pH-homeostasis

42

full compensation

restore pH normal, restore 20:1 ratio of HCO3:H2CO3; even with normal pH, the underlying renal or respiratory cause is not corrected

43

partial compensation

pH is approaching normal of 7.4

44

metabolic alkalosis

indicated by increased pH, increased HCO3; seen with hypochloremia, hypokalemia, loss of acid through vomiting, use of diuretics causing loss of H+, excess administration of sodium bicarb, and processes that remove acids from the body or produce excess base

45

H+ generation, bicarb secretion

renal compensation for metabolic alkalosis

46

decrease respiratory rate to increase pCO2

respiratory compensation for metabolic alkalosis

47

respiratory alkalosis

indicated by increased pH, increased pCO2; increase in ventilation (hyperventilation) causing excessive elimination of CO2 by lungs; seen in fever, hyperventilation, pulmonary fibrosis or embolism, hypoxia, sepsis of gram negative organisms which increase metabolic demands

48

excretion of HCO2 in urine to conserve H+ into the bloodstream

slow process of renal compensation for respiratory alkalosis

49

rebreathe CO2 by breathing into a bag to drop pH

respiratory compensation for respiratory alkalosis

50

metabolic acidosis

indicated by decreased pH and decreased HCO3; decrease in bicarbonate resulting in decreased pH; base removed from the body or excess acids are produced; dehydration due to diarrhea, renal tubular acidosis, hypokalemia, vomiting, DKA ketones present: hyponatremia, hyperglycemia, and hypokalemia present, corrected with insulin

51

hyperventilation to increase pCO2 along with a decrease in H+ to try to increase pH

quick pulmonary compensation for metabolic acidosis; pCO2 decreases 1-2 for each unit change in HCO3

52

increase H+ secretion and increase HCO3 generation

renal compensation for metabolic acidosis

53

respiratory acidosis

indicated by decrease in pH and increase in pCO2; decrease in alveolar ventilation, causing decreased elimination of CO2 by lungs; seen in hypoventilation where not enough CO2 is expelled so CO2 accumulates, COPD pneumonia, asthma, pulmonary edema, and drugs

54

excretion of H+ and retaining HCO3

slow renal compensation of respiratory acidosis

55

increase respiratory rate to decrease pCO2

respiratory compensation for respiratory acidosis

56

HCO3

based on Henderson-Hasselbalch equation; can be calculated when pH and pCO2 are known

57

carbonic acid concentration

can be calculated using solubility coefficient of CO2 in plasma at 37C

58

total carbon dioxide content-tCO2

bicarbonate plus carbonic acid plus associated CO2 with proteins

59

base excess

excess of insufficient HCO3 present; defined as the amount of H+ required to return pH of blood to 7.4 if pCO2 were adjusted to normal; estimated by an equation 0.93(HCO3-24.4+14.8(pH-7.4)) normal -2 to +2 mEq

60

0.93(HCO3-24.4+14.8(ph-7.4))

base excess equation

61

pO2 measurement

amperometric Clarke electrodes measure amount of current flow in circuit related to amount of O2 being reduced at cathode; sources of error: buildup of protein on material on surface of membrane, bacterial contamination within measuring chamber

62

pH measurement

Ag-AgCl electrode used to measure potential difference related to concentration of ion

63

pCO2 measurement

modified pH, the Severinghaus electrode; measures change in acid formation of carbonic acid based on pH changes

64

spectrophotometric determination of oxygen saturation

actual percent of oxyhemoglobin determined using co-oximeter designed to measure various hgb types since each has a characteristic absorbance curve

65

carboxyhemoglobin measurement

measured using spectrophotometric determination to obtain absorbance to compare with that of normal hemoglobin

66

methemoglobin

dysfunctional hgb because iron is in ferric form Fe3+

67

total CO2 - (pO2 x 0.03)

HCO3 calculated equation

68

80-100 mmHg

normal pO2 value

69

<40

pO2 value interpreted as severe hypoxemia

70

anion gap

normal 8-16 mmol/L; may indicate metabolic acidosis or increased due to lactic acid, ketones, methanol, ethylene glycol, salicylates, toxins, starvation, tylenol

71

partially compensated

compensating system is abnormal

72

uncompensated

compensating system is normal and not attempting to correct